Course reading and evidence

Objective: lytes-12

Extra potassium outside the cell narrows the gap between the resting and threshold potential of heart muscle, and the first thing that shows is faster, steeper repolarization — tall, peaked T waves with a narrow base. As the level climbs, conduction slows: the P wave flattens and disappears, the PR interval stretches, the QRS widens, and the last stop is a sine wave and then asystole or ventricular fibrillation . This is the classic teaching sequence, not a reliable progression in an individual patient: dangerous conduction changes may appear without earlier peaked T waves, and a normal ECG does not exclude severe hyperkalemia.

Source-supported decision rule; faculty review pending.

• UKKA hyperkalemia guideline July 2026 — 14.1–14.2, 15.2–15.3, 16.2a–b

Question · Answer and explanation

Objective: lytes-01

The jugular vein is a window on the pressure in the right side of the heart. When the circulation is overfilled, that pressure rises and the vein stays full high up the neck. Pair it with the lungs (crackles), the legs (pitting edema), the blood pressure (often high) and the weight trend, and the exam gives one answer. One liter of retained fluid weighs about one kilogram, which is why the dialysis unit weighs patients before and after every run.

Clinical application or calculation based on the cited principles; faculty review pending.

• ESC guideline for the management of heart failure2026 — 5.1 Table7; 6.1.3.1; RecommendationTable5; 7.4.2; 7.5.4
• KDIGO AKI guideline2012 — 2.3, printedp27; 2.5 Table13, p35

Question · Answer and explanation

Objective: lytes-13

Hyperkalemia treatment has three jobs that run in parallel . Stabilize — calcium protects the heart muscle membrane but changes the potassium not at all. Shift — insulin (with glucose so the patient does not go low) and a beta-agonist drive potassium into cells for a few hours; the total amount in the body is unchanged and it will come back out. Remove — a loop diuretic if the kidneys make urine, a gut binder, or dialysis. Only the third group lowers total-body potassium, and in a patient with no kidney function, dialysis is the only one that works fast.

Source-supported decision rule; faculty review pending.

• UKKA hyperkalemia guideline July 2026 — 16.3.1–16.6.2; 17.1.1–17.2

Question · Answer and explanation

Objective: lytes-12, lytes-13

Hemolysis adds potassium to the tube after the blood has left the body; it cannot change what the heart has been bathing in. A QRS of 148 ms with vanishing P waves is the heart telling you its potassium is dangerously high, whatever the tube says. A convincing ECG is treated the moment you see it — calcium gluconate 10%, 10 mL (1 g) over 2–3 minutes, repeated in 5 minutes if the QRS has not narrowed — and the repeat sample is sent at the same time, not instead. Calcium works in minutes and lasts only 30–60 minutes, so the shift and removal steps start right behind it: stabilize, shift, remove, in parallel, is the sequence every emergency guideline teaches .

Source-supported decision rule; faculty review pending.

• UKKA hyperkalemia guideline July 2026 — 14.1–14.2, 15.2–15.3, 16.2a–b
• UKKA hyperkalemia guideline July 2026 — 18.1–18.3; 19.1–19.6
• Hyperkalemia management in the emergency department: expert panel consensus 2021 — 2 Step2; 1.6.1 Calcium

Question · Answer and explanation

Objective: lytes-14

Trimethoprim inhibits distal-nephron ENaC and can impair renal potassium secretion; lisinopril and the potassium-chloride salt substitute add risk. With very little residual kidney function, the size of trimethoprim's renal contribution is uncertain. The missed dialysis sessions and potassium load are the dominant established explanations. Stop the avoidable contributors and arrange definitive potassium removal.

Clinical application or calculation based on the cited principles; faculty review pending.

• BACTRIM US prescribing information — Precautions: Electrolyte abnormalities; Geriatric use
• UKKA hyperkalemia guideline July 2026 — 18.1–18.3; 19.1–19.6

Question · Answer and explanation

Objective: aki-22, aki-24

The AEIOU mnemonic names the reasons to dialyze tonight rather than tomorrow: Acidosis that is severe and refractory, Electrolytes — refractory hyperkalemia, especially with ECG changes, Intoxication with a dialyzable drug, Overload — pulmonary edema that diuretics cannot fix, and Uremia with symptoms (pericarditis, confusion, bleeding, intractable nausea). Potassium 7.3 with a wide QRS is the E, and in a man with no kidney function it is unlikely to be controlled durably by shifting treatment alone — medical therapy only hides it for a few hours. He also has the O (pulmonary edema, no meaningful urine to diurese) and early U (anorexia, nausea, metallic taste). The A is present but moderate (pH 7.24, appropriately compensated) and will correct with the run; on its own it would not force dialysis tonight.

Source-supported decision rule; faculty review pending.

• UKKA hyperkalemia guideline July 2026 — 18.1–18.3; 19.1–19.6
• KDIGO AKI guideline 2012 — 5.1.1–5.1.2

Question · Answer and explanation

Objective: lytes-01, aki-22

The combined weight gain, high JVP, crackles, edema and chest film support severe congestion. With only a small residual urine volume, diuretics cannot be relied on for prompt adequate removal. Urgent dialysis provides definitive potassium and volume treatment. Some patients with residual kidney function still respond to loops; this is not a rule that every low-output dialysis patient has zero response at every dose. Support breathing and avoid unnecessary IV volume while arranging treatment.

Clinical application or calculation based on the cited principles; faculty review pending.

• UKKA hyperkalemia guideline July 2026 — 18.1–18.3; 19.1–19.6

Question · Answer and explanation

Objective: lytes-13

Calcium bought 30–60 minutes of membrane protection and changed the potassium by nothing. Dialysis is not an event that happens when you say the word — a nurse has to drive in, a machine has to be primed and tested, the access has to be cannulated — so the gap is covered by the shift therapies that every emergency-department bundle agrees on : insulin with dextrose (onset about 15 minutes, drops potassium 0.6–1.0 mEq/L for a few hours) and high-dose nebulized albuterol — 10–20 mg, far above a bronchodilator dose, which lowers potassium a further 0.5–1.0 mEq/L in dialysis patients ; the two effects are additive . A binder started now has begun working by the time the run ends, which matters because potassium rebounds when the shift wears off and after dialysis. Check glucose before insulin and at 30, 60, 90, 120, 180, 240, 300 and 360 minutes afterward; delayed hypoglycemia in kidney failure requires the full monitoring schedule (UKKA 2026, Guideline 17.2). And recheck the ECG and potassium: the one-hour value tells you whether the shift took.

Source-supported decision rule; faculty review pending.

• Acute hyperkalemia in the emergency department: KDIGO conference report 2020 — Figure3, p334
• UKKA hyperkalemia guideline July 2026 — 16.3.1–16.6.2; 17.1.1–17.2

Question · Answer and explanation

Objective: lytes-13, aki-22

Insulin and albuterol move potassium into cells; they remove none of it. A fall of about one point in the first hour is exactly what the shift is expected to do, and it wears off over the next few hours, so the number says nothing about the total-body excess. Nothing that made tonight's run necessary has changed: no meaningful urine, 4 kg over dry weight with pulmonary edema, BUN 110 and bicarbonate 15.

Clinical application or calculation based on the cited principles; faculty review pending.

• UKKA hyperkalemia guideline July 2026 — 18.1–18.3; 19.1–19.6
• UKKA hyperkalemia guideline July 2026 — 16.3.1–16.6.2; 17.1.1–17.2

Question · Answer and explanation

Objective: ckd-23

Protect his functioning fistula and preserve vessels for future access. KDOQI 2019 uses an individualized ESKD Life-Plan rather than a universal fistula-first hierarchy. A mature fistula has important advantages for this patient, but another patient may appropriately receive a graft, catheter, peritoneal dialysis or transplant. Use the right arm for necessary routine peripheral access here; avoid a PICC without nephrology/access-team review. Routine fistula cannulation belongs to trained dialysis personnel.

Source-supported decision rule; faculty review pending.

• KDOQI Vascular Access 2019 Update — 1.1–1.3, 2.1; 6.1, 6.6, 6.10

Question · Answer and explanation

Objective: lytes-04, lytes-05

The matching runs 1 = hypovolemic (ADH on because the body is dry; the kidney saves sodium, so urine Na is low), 2 = SIADH (ADH on inappropriately in a patient with normal volume, so the kidney does not save sodium and urine Na is high), 3 = low-solute or beer potomania (ADH is off — urine osmolality under 100 means the kidney is diluting as hard as it can, but with almost no solute to excrete it cannot unload the water), 4 = hypervolemic (ADH on because the heart cannot deliver volume to the kidney; sodium is retained, so urine Na is low). SIADH is the only branch that pairs a concentrated urine with a high urine sodium and a normal volume exam — that is Patient 2.

Clinical application or calculation based on the cited principles; faculty review pending.

• European hyponatraemia guideline: official short version 2014 — 2.2–2.3, pp7–9; Tables3–4, pp16–17; 3.4

Question · Answer and explanation

Objective: lytes-04

Urine osmolality 410 is inappropriately concentrated during hypotonicity. ADH activity is a common explanation, but this is not a direct hormone assay: thiazides and kidney disease can also impair dilution. Use medication history, kidney function, volume findings and the clinical context to determine why the patient cannot excrete the water load.

Clinical application or calculation based on the cited principles; faculty review pending.

• European hyponatraemia guideline: official short version 2014 — 2.2–2.3, pp7–9; Tables3–4, pp16–17; 3.4

Question · Answer and explanation

Objective: lytes-10

This is the most common hypernatremia in the hospital: a patient who cannot get to water (dementia) plus extra free-water loss (fever, insensible loss through skin and lungs). Her urine osmolality of 720 says the kidney is doing its job — ADH is present and the collecting duct is responding — so this is not diabetes insipidus. The free-water deficit: total body water in an elderly woman = 0.45 × 50 kg = 22.5 L; deficit = TBW × (Na/140 − 1) = 22.5 × (158/140 − 1) = 22.5 × 0.129 ≈ 2.9 L. Replace it with water by mouth or feeding tube if she can take it, otherwise D5W, plus her ongoing losses, and bring the sodium down no faster than 10–12 mEq/L in 24 hours (about 0.5 mEq/L per hour) — a brain that has adapted to a high sodium swells if you dilute it too fast. If she were hypotensive you would give isotonic saline first for the circulation and switch to free water once stable.

Clinical application or calculation based on the cited principles; faculty review pending.

• Society for Endocrinology inpatient cranial diabetes insipidus guidance 2018 — Management of decompensated CDI, section5; Box2

Question · Answer and explanation

Objective: lytes-01

Orthostatic blood-pressure and pulse changes, together with measured weight loss, low JVP and the drug history, support volume depletion here. No single physical sign proves the volume state. Orthostasis may also reflect autonomic disease or medications, so it does not automatically exclude coexisting SIADH. BUN:creatinine and hemoconcentration are supportive contextual findings, not definitive volume tests.

Clinical application or calculation based on the cited principles; faculty review pending.

• European hyponatraemia guideline: official short version 2014 — 2.2–2.3, pp7–9; Tables3–4, pp16–17; 3.4

Question · Answer and explanation

Objective: lytes-04

Step one of every hyponatremia work-up is to prove the low sodium is a real water problem. A low measured serum osmolality (248) does that: it excludes pseudohyponatremia (a lab artifact from very high lipids or proteins, in which the osmolality is normal) and hypertonic hyponatremia (glucose or mannitol pulling water into the blood, in which the osmolality is high). The glucose correction is worth saying out loud every time: corrected Na = measured Na + 1.6 × (glucose − 100)/100 when glucose is 400 or below — here 118 + 1.6 × 0.08 ≈ 118.1, so the 118 stands. Then the work-up runs in order: urine osmolality (is ADH on?), urine sodium (what is the kidney doing with salt — remembering she is on a diuretic), TSH and cortisol (hypothyroidism and adrenal insufficiency both impair water excretion and must be excluded before anyone says "SIADH"), magnesium (her potassium is 2.8), and a medication review — thiazide, SSRI and NSAID are all on her list.

Clinical application or calculation based on the cited principles; faculty review pending.

• European hyponatraemia guideline: official short version 2014 — 2.2–2.3, pp7–9; Tables3–4, pp16–17; 3.4

Question · Answer and explanation

Objective: lytes-06

The new thiazide is the leading contributor to hypotonic hyponatremia with potassium, magnesium and chloride depletion. It impairs urinary dilution and can produce sodium loss and hypovolemia; this patient has several findings supporting depletion. Sertraline, NSAID exposure, low solute intake and excess water may contribute. Concentrated urine shows impaired water excretion but is not a direct ADH assay.

Clinical application or calculation based on the cited principles; faculty review pending.

• European hyponatraemia guideline: official short version 2014 — 2.2–2.3, pp7–9; Tables3–4, pp16–17; 3.4
• Hydrochlorothiazide US prescribing information — Precautions: Fluid and electrolyte balance

Question · Answer and explanation

Objective: lytes-11, lytes-18, lytes-25

Read the BMP as a pattern: thiazides waste potassium and magnesium in the distal tubule and waste chloride with the sodium, and volume contraction then makes the kidney hold on to bicarbonate — exactly her panel (K 2.8, HCO₃ 34, Cl 74, Mg 1.4). The alkalosis is the chloride-depletion ("contraction," saline-responsive) type, which fixes itself once chloride and volume are given back and the cause is removed. Magnesium comes first in your thinking because without it the kidney keeps wasting potassium and the potassium you give will not stay in — so start magnesium sulfate 2 g IV over 2 hours first, or alongside the potassium; with a potassium under 3.0 and an ECG change, do not delay the potassium for the magnesium to finish. The potassium goes IV because she is nauseated, under 3.0 and has an ECG change: diluted in isotonic saline (avoid unnecessary dextrose during initial potassium replacement because insulin release can shift potassium into cells), at 10 mEq/h or less through a peripheral line, on a cardiac monitor, with a recheck in 4–6 hours.

Clinical application or calculation based on the cited principles; faculty review pending.

• Hydrochlorothiazide US prescribing information — Precautions: Fluid and electrolyte balance
• European hyponatraemia guideline: official short version 2014 — 2.2–2.3, pp7–9; Tables3–4, pp16–17; 3.4

Question · Answer and explanation

Objective: lytes-08, lytes-09

Confusion can be a moderately severe symptom of hypotonic hyponatremia. A single 150-mL 3% bolus over 20 minutes is a guideline-supported option when symptoms are attributed to hyponatremia; reassess symptoms and sodium promptly. This is not an instruction to normalize sodium or repeat boluses solely because it is below 120. Stop the causative drugs and address volume and potassium deficits, counting every treatment toward the correction limit. The treating senior clinician selects and documents the monitored protocol.

Source-supported decision rule; faculty review pending.

• Society for Endocrinology emergency hyponatraemia guidance 2022 — Treatment recommendation 1(a–d), Figure1

Question · Answer and explanation

Objective: lytes-06

In a patient who is not on a diuretic, a urine sodium of 55 in hypotonic hyponatremia is a real finding: a dry kidney should be saving every milliequivalent (urine Na under 20–30), so a high value would say the kidney is not short of volume and push you toward SIADH, adrenal insufficiency or a salt-wasting kidney. On a thiazide, the drug forces the kidney to waste sodium whether the body is dry or not — a urine sodium above 30 is the drug's signature, not evidence of euvolemia, so it cannot move the hypothesis in either direction; it is uninterpretable, and the volume exam and the drug timeline decide. That is the conditional part the night resident missed. Two bedside facts settle the case: she was orthostatic and 2.5 kg down, and a thiazide was started three weeks ago in a woman whose sodium was 137 before it — nothing in a urine cup outranks those.

Clinical application or calculation based on the cited principles; faculty review pending.

• European hyponatraemia guideline: official short version 2014 — 2.2–2.3, pp7–9; Tables3–4, pp16–17; 3.4

Question · Answer and explanation

Objective: lytes-09

She is already up 7 mEq/L in 10 hours and is beginning to excrete more water. Stop saline, continue necessary potassium cautiously by mouth, measure sodium every two hours, follow urine output closely and call nephrology now. Hypokalemia and poor intake increase concern for osmotic demyelination; aim for a modest rise and do not exceed 8 mEq/L in 24 hours in this high-risk patient. Specialist-directed desmopressin and/or electrolyte-free water may be needed before the ceiling is crossed.

Clinical application or calculation based on the cited principles; faculty review pending.

• Society for Endocrinology emergency hyponatraemia guidance 2022 — Treatment recommendation 1(a–d), Figure1

Question · Answer and explanation

Objective: lytes-27, htn-cardiorenal-06

Avoid another thiazide in this patient after severe symptomatic hyponatremia. Susceptibility can recur on rechallenge; changing to a different thiazide does not reliably remove that risk. Record the adverse effect and select an alternative class with monitoring. Her hypertension is real (stage 2, confirmed by home readings) and the 2025 guideline still treats it at 76; what changes in a frail older adult is how: pick a class without electrolyte effects, start low, titrate slowly, check the standing pressure at every visit, and keep the target of under 130/80 only if she gets there without orthostatic symptoms or a systolic below 110 standing. Amlodipine (a dihydropyridine calcium channel blocker — no sodium, potassium or magnesium effect; watch for ankle swelling) and an ACE inhibitor (lisinopril — needs a BMP at 1–2 weeks for potassium and creatinine) are both first-line classes and both reasonable here; a single agent started low is the frail-adult approach even though stage 2 hypertension would usually start two drugs in a younger patient. Then the system fix: a BMP 1–2 weeks after starting or changing any diuretic — she was booked for six weeks — and written instructions that "stay hydrated" does not mean nine glasses of water.

Clinical application or calculation based on the cited principles; faculty review pending.

• Thiazide-induced hyponatremia: reproducibility by single-dose rechallenge1989 — Abstract: patients, intervention and results

Question · Answer and explanation

Objective: lytes-06

The dilute urine shows that ADH is largely suppressed. Excreting water still requires enough urinary solute; very little protein and salt can limit water clearance even when the kidney dilutes appropriately. Assess nutrition and intake, correct cautiously, and watch for brisk water diuresis when solute is restored.

Clinical application or calculation based on the cited principles; faculty review pending.

• European hyponatraemia guideline: official short version 2014 — 2.2–2.3, pp7–9; Tables3–4, pp16–17; 3.4

Question · Answer and explanation

Objective: lytes-21

AG = Na − (Cl + HCO₃) = 138 − (104 + 18) = 16. Albumin is the main unmeasured anion that normally fills the gap. When albumin is low, the gap you measure is artificially small, so you add it back: 2.5 mEq/L for every 1 g/dL of albumin below 4.0. Here that is 2.5 × 2 = 5, giving a corrected gap of 21 — a real high-gap acidosis that the uncorrected number would have called borderline.

Clinical application or calculation based on the cited principles; faculty review pending.

• Anion gap and hypoalbuminemia: original study1998 — Abstract: Methods, Results, Conclusions

Question · Answer and explanation

Objective: aki-01

KDIGO 2012 stages by whichever criterion gives the higher stage. 1.7 ÷ 0.8 = 2.1 times baseline, which is stage 2 (2.0–2.9×). The ≥0.3 mg/dL rule also fires, but it only reaches stage 1, and the higher stage wins. Urine output is above 0.5 mL/kg/h, so it adds nothing here.

Source-supported decision rule; faculty review pending.

• KDIGO AKI guideline 2012 — 2.1.1–2.1.2; Table2, printedp19

Question · Answer and explanation

Objective: aki-15, htn-cardiorenal-25

The sick-day hold list (SADMANS — sulfonylureas, ACE inhibitors, diuretics, metformin, ARBs and ARNI, NSAIDs, SGLT2 inhibitors; mineralocorticoid antagonists are held too) covers drugs that lower kidney perfusion, accumulate when GFR falls, or add volume loss during an illness that is already draining him. Beta-blockers are the opposite case: stopping one abruptly causes rebound tachycardia and hypertension. He continues metoprolol unless he is frankly hypotensive or bradycardic.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO CKD guideline 2024 — 3.6.3–3.6.5; 3.7.1–3.7.3

Question · Answer and explanation

Objective: lytes-26

On an SGLT2 inhibitor the glucose is the one finding whose meaning is conditional. The drug holds the blood glucose near normal by dumping it in the urine while ketoacid production runs unopposed, so a glucose of 206 carries no information about whether ketoacidosis is present — it is the expected glucose in SGLT2 inhibitor ketoacidosis. The hypothesis stays exactly where the vomiting, the fruity breath and the Kussmaul breathing put it; what moves it are the gap (already 34) and a ketone measurement — Q6 asks which one. Off an SGLT2 inhibitor the same glucose would be reassuring; that is the circumstance the student must notice, and the one the resident missed.

Clinical application or calculation based on the cited principles; faculty review pending.

• Hyperglycemic Crises in Adults With Diabetes: Consensus Report 2024 — Diagnostic criteria; treatment subsections Fluid therapy, Insulin therapy, Potassium, Phosphate; Criteria for resolution; SGLT2 special population

Question · Answer and explanation

Objective: lytes-20, lytes-21, lytes-22

Three lines. Gap: 134 − (86 + 14) = 34, and albumin 4.0 needs no correction. Winter's formula — the pCO₂ the lungs should produce for this bicarbonate — is 1.5 × 14 + 8 = 29 ± 2, so the actual 30 sits inside the window: compensation is appropriate and there is no respiratory disorder. Delta-delta: ΔAG = 34 − 12 = 22 against ΔHCO₃ = 24 − 14 = 10, ratio 2.2 — above 2 means something is holding the bicarbonate up, and three days of vomiting hydrochloric acid (the chloride of 86 is its fingerprint) is a metabolic alkalosis hidden inside the acidosis. Without it his bicarbonate would be about 24 − 22 = 2: he is sicker than 14 looks.

Clinical application or calculation based on the cited principles; faculty review pending.

• Anion gap and hypoalbuminemia: original study1998 — Abstract: Methods, Results, Conclusions
• Hyperglycemic Crises in Adults With Diabetes: Consensus Report 2024 — Diagnostic criteria; treatment subsections Fluid therapy, Insulin therapy, Potassium, Phosphate; Criteria for resolution; SGLT2 special population

Question · Answer and explanation

Objective: lytes-26

Run the gap differential (MUDPILES — methanol, uremia, DKA/ketones, propylene glycol, isoniazid/iron, lactate, ethylene glycol, salicylates) against what you already have: lactate 1.6 removes lactic acidosis, including metformin-associated lactic acidosis from the other drug on his list; osmolal gap 4 does not suggest a large unmetabolized alcohol load, but cannot exclude a late toxic-alcohol exposure; creatinine 1.9 is unlikely to explain this large gap by uremia alone. The SGLT2 exposure, fasting and symptoms make blood ketone measurement the best next test. The dominant ketoacid in DKA is β-hydroxybutyrate, measured in blood; the urine dipstick's nitroprusside reaction detects acetoacetate (and weakly acetone) and does not react with β-hydroxybutyrate at all, so the dipstick reads falsely low early in the illness. A serum β-hydroxybutyrate of 3.0 mmol/L or more is diagnostic-range ketonemia regardless of the glucose. On an SGLT2 inhibitor the drug dumps glucose into the urine, so the blood glucose stays near normal while ketoacid production runs unchecked — euglycemic diabetic ketoacidosis (the classic definition is a ketoacidosis at a glucose under 250 mg/dL; the 2024 consensus report draws the line at 200 — either way, the glucose is not the test).

Source-supported decision rule; faculty review pending.

• Hyperglycemic Crises in Adults With Diabetes: Consensus Report 2024 — Diagnostic criteria; treatment subsections Fluid therapy, Insulin therapy, Potassium, Phosphate; Criteria for resolution; SGLT2 special population

Question · Answer and explanation

Objective: aki-01, aki-02, aki-04

Stage by the ratio: 1.9 ÷ 1.0 = 1.9, inside the stage 1 band (1.5–1.9×); stage 2 starts at 2.0×. The compartment is prerenal on every line — losses, orthostasis, a 4 kg drop, BUN:creatinine over 20:1 with nothing else raising urea (no GI bleed, no steroids), concentrated urine, bland sediment with hyaline casts. The treatment of prerenal AKI is to restore perfusion with isotonic crystalloid and then look again — creatinine, urine output, orthostatics — in 12–24 hours. The hold-list drugs (lisinopril, metformin, empagliflozin) stay off while the kidney recovers.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO AKI guideline 2012 — 2.1.1–2.1.2; Table2, printedp19
• KDIGO CKD guideline 2024 — 1.3 GFR evaluation, pS175–S180; errors with non-steady state

Question · Answer and explanation

Objective: lytes-11, lytes-26

At K 3.1, delay insulin and replace potassium with monitoring until K is above 3.5 mmol/L. The 2024 consensus describes starting replacement at 10 mmol/h; a higher rate requires the local monitored protocol and appropriate access. Once safe, give insulin with dextrose because glucose is already below 250 mg/dL. Recheck potassium promptly.

Source-supported decision rule; faculty review pending.

• Hyperglycemic Crises in Adults With Diabetes: Consensus Report 2024 — Diagnostic criteria; treatment subsections Fluid therapy, Insulin therapy, Potassium, Phosphate; Criteria for resolution; SGLT2 special population

Question · Answer and explanation

Objective: lytes-02, lytes-23

The chloride tells you what the saline did. 0.9 % saline carries 154 mEq/L of chloride against a plasma chloride of about 100; after several liters the excess chloride displaces bicarbonate and produces a hyperchloremic (non-gap) metabolic acidosis — the falling delta-delta is the arithmetic of exactly that. Balanced crystalloids (lactated Ringer's, Plasma-Lyte) carry about 100–110 mEq/L of chloride plus a buffer (lactate or acetate) the liver converts to bicarbonate; in large volumes they avoid the chloride load, and the current DKA consensus prefers them. He still needs volume, dextrose (glucose is 164 and insulin is running) and potassium (target ≥4.0), so those ride in the new fluid.

Source-supported decision rule; faculty review pending.

• Hyperglycemic Crises in Adults With Diabetes: Consensus Report 2024 — Diagnostic criteria; treatment subsections Fluid therapy, Insulin therapy, Potassium, Phosphate; Criteria for resolution; SGLT2 special population

Question · Answer and explanation

Objective: lytes-23

Resolved ketonemia, chloride 110 after a large saline load, normal potassium and recovering kidney function favor transient hyperchloremic acidosis from saline and urinary ketoanion loss. A negative urine anion gap supports ammonium excretion in a suitable setting but is an imperfect surrogate; ketoanions and other unmeasured urinary ions can confound it. Urine pH 5.2 argues against classic distal RTA but is not a universal test of total acid excretion. Recheck rather than reflexively prescribe alkali or restart a DKA infusion.

Clinical application or calculation based on the cited principles; faculty review pending.

• Hyperglycemic Crises in Adults With Diabetes: Consensus Report 2024 — Diagnostic criteria; treatment subsections Fluid therapy, Insulin therapy, Potassium, Phosphate; Criteria for resolution; SGLT2 special population

Question · Answer and explanation

Objective: ckd-04

The equation was built from people with stable kidney function. When creatinine is rising, the number in the blood lags days behind the fall in filtration, so the eGFR printed on the report is far too flattering. Write "eGFR not valid — creatinine is moving" and follow the creatinine trend instead. The other known limits are extremes of muscle mass (body-builders, amputees, frail elders), drugs that block creatinine secretion (trimethoprim, cimetidine), creatine supplements and pregnancy; cystatin C is the confirmatory test when the creatinine estimate is in doubt.

Source-supported decision rule; faculty review pending.

• KDIGO CKD guideline 2024 — 1.3 GFR evaluation, pS175–S180; errors with non-steady state

Question · Answer and explanation

Objective: htn-cardiorenal-01

Use quiet seated rest, supported back and feet, the arm supported at heart level, and an appropriately sized validated cuff. Obtain repeated readings separated by 1–2 minutes and average them. D follows those requirements. Technique errors can materially distort pressure, but their effects vary and should not be added as fixed numerical corrections to a patient's result.

Clinical application or calculation based on the cited principles; faculty review pending.

• Measurement of blood pressure in humans: AHA scientific statement2019 — Table5

Question · Answer and explanation

Objective: ckd-03

The dipstick reads protein by concentration, with a chemistry that responds mainly to albumin and poorly at low levels, so it turns reliably positive only around the A3 line (300 mg/g) — a trace-or-greater strip catches variable and insufficient to exclude A2 of A2 patients (36 % sensitivity), and a dilute urine reads lower still. The UACR measures albumin by immunoassay and divides by creatinine, so dilution does not fool it, and 30–300 mg/g is A2 whatever the strip says. That is why KDIGO (the international kidney guideline group) stages albuminuria by the ratio and treats the dipstick as a screen: a trace or negative strip in a patient at risk for CKD is a reason to send the ratio, not reassurance. One ratio is a data point, not a trend — confirm it on a repeat first-morning sample before acting on it.

Source-supported decision rule; faculty review pending.

• KDIGO CKD guideline 2024 — Tables1–3, pS137; 1.1 chronicity/albuminuria evaluation

Question · Answer and explanation

Objective: htn-cardiorenal-01, htn-cardiorenal-02

Remeasure using correct technique before making a routine medication change, then compare a properly collected home BP average. The initial reading followed exertion, talking and unsupported posture with an undersized cuff. Those errors can bias the result but do not establish a predictable additive error. A later controlled reading of 144/88 remains above target and still requires follow-up and treatment review.

Clinical application or calculation based on the cited principles; faculty review pending.

• Measurement of blood pressure in humans: AHA scientific statement2019 — Table5

Question · Answer and explanation

Objective: ckd-01, ckd-02

eGFR34 is G3b and UACR180 is A2; the combination is in the very-high-risk red cell. The prior abnormality establishes chronicity. Monitoring frequency and referral depend on risk, trajectory and complications. A red cell does not by itself mandate referral within one month; her difficult BP, anemia, diagnostic uncertainty and later KFRE support referral. The decline from eGFR38 to34 over two years is approximately2mL/min/1.73m² per year.

Source-supported decision rule; faculty review pending.

• KDIGO CKD guideline 2024 — Tables1–3, pS137; 1.1 chronicity/albuminuria evaluation

Question · Answer and explanation

Objective: ckd-05, ckd-07, htn-cardiorenal-16

"Hypertensive nephrosclerosis" (long-standing high pressure scarring the small arteries and the glomeruli behind them) is a diagnosis of exclusion — it is listed as the second cause of kidney failure in the United States, yet the clinical criteria for it have about 13 % sensitivity and it is rarely confirmed by biopsy, so much of what carries the label is another kidney disease with hypertension riding along. What fits: a long hypertension history, target-organ damage elsewhere (her LVH), a bland urine (no blood, no cellular casts), low-grade albuminuria (A2, under about 1 g/day), a slow slope, and two symmetric, smooth kidneys. What un-fits: A3 albuminuria or more than 1 g/day of protein, hematuria or red-cell casts, white-cell casts, a decline over 5 mL/min per year, onset young, a family history of kidney disease, or systemic symptoms. The three first-line tests answer exactly those questions — microscopy for cells and casts, a repeat UACR because one value is not a trend, an ultrasound for size, symmetry, cysts and obstruction — and if they come back clean the honest wording is "CKD, presumed nephrosclerosis," held loosely.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO CKD guideline2024 — 1.1.4.1; Table6 and Figure8, pS174

Question · Answer and explanation

Objective: ckd-14

Microcytosis and high RDW suggest iron deficiency, which can coexist with CKD-related erythropoietin deficiency. Check ferritin and TSAT and investigate blood loss and other reversible causes before an ESA. A negative stool blood test does not exclude gastrointestinal blood loss and should not gate indicated GI evaluation. ESA initiation in nondialysis CKD is individualized after reversible causes are addressed; KDIGO 2026 recommends an ESA-treated hemoglobin target below 11.5 g/dL.

Source-supported decision rule; faculty review pending.

• KDIGO Anemia in CKD guideline2026 — 2.3; evaluation and ESA target recommendations

Question · Answer and explanation

Objective: ckd-16

The gap is 139 − (108 + 19) = 12. CKD-related acid retention is plausible, but a chemistry bicarbonate alone cannot exclude respiratory alkalosis; repeat and obtain a blood gas if the clinical distinction remains uncertain. KDIGO 2024 Practice Points 3.10.1–2 advise considering treatment to prevent clinically important acidosis, giving bicarbonate below 18 mmol/L as an example. A stable value of 19 does not mandate sodium bicarbonate. Discuss dietary measures or a monitored alkali trial according to persistence, symptoms, potassium, blood pressure and volume. Do not promise that alkali will slow CKD progression.

Source-supported decision rule; faculty review pending.

• KDIGO CKD guideline 2024 — 3.10.1–3.10.2, pS222

Question · Answer and explanation

Objective: ckd-15

This is the early pattern of CKD mineral and bone disorder (CKD-MBD): fewer nephrons retain phosphate, PTH rises to push it out, and the kidney makes less active vitamin D, so calcium absorption falls and PTH rises further — at G3b the serum phosphorus is usually still near normal (hers is barely over the line) while the PTH is already up. What primary care owns: the nutritional deficiency (25-OH D under 20 is deficiency, 20–29 insufficiency; cholecalciferol using a local replacement regimen and follow-up level), the diet (phosphate additives in processed food and colas are the first target; a renal dietitian helps), and the recheck schedule for G3b — calcium and phosphorus every 6–12 months when stable, PTH at intervals set by the trend. What nephrology owns: there is no established PTH target in non-dialysis CKD, so a single PTH of 118 is not a calcitriol indication; active vitamin D is reserved for severe, progressive hyperparathyroidism after the modifiable factors are fixed, and calcimimetics (drugs that quiet the parathyroid, used on dialysis) are not a G3b drug. The distinguishing feature is the vitamin D level — treat the deficiency you can measure, and follow the PTH you cannot yet target.

Source-supported decision rule; faculty review pending.

• KDIGO CKD-MBD guideline 2017 — 3.1.1–3.1.4; 4.2.1–4.2.2, p33

Question · Answer and explanation

Objective: ckd-14

Her TSAT of 13% together with ferritin 48 ng/mL supports systemic iron deficiency in non-dialysis CKD. TSAT below 20% alone does not distinguish depleted iron stores from iron-restricted erythropoiesis. The ferritin is the finding whose meaning is conditional: 48 sits inside the lab's range, but that range is for people without kidney disease — KDIGO 2026 starts iron in non-dialysis CKD at a ferritin under 100 with TSAT under 40 % — and ferritin rises with inflammation, so 48 if anything overstates her stores. A positive guaiac card in a postmenopausal woman is gastrointestinal blood loss until proven otherwise, though her iron deficiency would have earned the gastroenterology referral without it. So "CKD alone" is much less likely — but not excluded: at eGFR 34 her erythropoietin reserve is limited and will cap how far iron can take her. The honest reading is "iron deficiency from GI loss on top of CKD": oral iron and a gastroenterology referral now, any ESA left to nephrology once the iron is replete.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO Anemia in CKD guideline2026 — 2.3; evaluation and ESA target recommendations

Question · Answer and explanation

Objective: htn-cardiorenal-10, ckd-19, structural-20

First remove oral ibuprofen and reassess the home pressure, adherence and diuretic regimen. Refill history supports adherence but does not prove it, and hydrochlorothiazide 25 mg is not its maximum possible dose. Chlorthalidone is an option that can remain effective at low GFR; use a low starting dose and recheck sodium, potassium and creatinine within 1–2 weeks. This is apparent treatment-resistant hypertension until reversible causes and technique are addressed.

Clinical application or calculation based on the cited principles; faculty review pending.

• Chlorthalidone for hypertension in advanced chronic kidney disease2021 — Abstract: Methods and Results
• Ibuprofen US prescribing information — Warnings: Renal effects

Question · Answer and explanation

Objective: ckd-21, htn-cardiorenal-02, htn-cardiorenal-04

The target for an adult with CKD is under 130/80 (2025 AHA/ACC and ADA; KDIGO 2021 goes further to a standardized-office systolic under 120 when tolerated, a number that presumes a measurement most clinics do not make), and the home threshold is the same 130/80 — there is no looser home target, so 138/86 is better and it is not goal. Referral is not a failure, it is the next step her chart already earned twice over: "uncontrolled hypertension despite three drugs" is an urgent referral on the staging handout's chart, and G3b with albuminuria is a referral within a month. By KDIGO 2024 she qualifies on the kidney-failure risk equation (5-year risk about 11 % at eGFR 34, UACR 180, age 58, female — well above the 3–5 % threshold); the local chart's G3b-with-albuminuria and uncontrolled-hypertension rows are the same decision stated more simply. Send the data that lets nephrology start where you finished — the creatinine trend (1.6 in 2024, 1.72 now), the two UACRs, the microscopy, the ultrasound, the home log, the iron studies, the bicarbonate, the PTH and vitamin D, and the medication list with the ibuprofen on it — and keep counselling while she waits.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO CKD guideline 2024 — 2.2.1–2.2.3, pS156; Figure48; 5.4.1 and Table41

Question · Answer and explanation

Objective: ckd-26

CKD increases cardiovascular risk. KDIGO 2024 Recommendation 3.15.1.1 recommends a statin or statin/ezetimibe for adults aged at least 50 with eGFR below 60 who are not receiving chronic dialysis or a transplant. Her modest LDL does not remove that indication. Choose the regimen with her after reviewing interactions, tolerance and preferences.

Source-supported decision rule; faculty review pending.

• KDIGO CKD guideline2024 — 3.15.1.1; 3.15.2.1, pS234

Question · Answer and explanation

Objective: ckd-02

eGFR 30–44 is G3b. UACR above 300 mg/g is A3 — "severely increased" albuminuria, the same range as the old word "macroalbuminuria." Two values more than three months apart make it chronic. On the KDIGO heat map G3b with A3 is the red cell: very high risk of progression and of cardiovascular events, and a referral trigger on its own.

Source-supported decision rule; faculty review pending.

• KDIGO CKD guideline 2024 — Tables1–3, pS137; 1.1 chronicity/albuminuria evaluation

Question · Answer and explanation

Objective: structural-23

Metformin is cleared by the kidney. The FDA label and KDIGO 2022 together give three eGFR bands: do not start below 45; between 30 and 45 reassess and halve the dose (KDIGO: maximum 1,000 mg a day — for him, 500 mg twice daily); stop below 30. The feared complication — metformin-associated lactic acidosis — is rare and is a disease of accumulation, so the dose is matched to clearance and the drug is held whenever clearance may fall suddenly (vomiting, dehydration, contrast with an eGFR below 30 or an AKI, surgery).

Clinical application or calculation based on the cited principles; faculty review pending.

• Metformin US prescribing information — 2.4–2.5

Question · Answer and explanation

Objective: ckd-11, ckd-12, ckd-13

The four pillars of diabetic kidney disease are RAAS blockade (one ACE inhibitor or ARB), an SGLT2 inhibitor, the nonsteroidal mineralocorticoid receptor antagonist finerenone, and a GLP-1 receptor agonist. Each lowers albuminuria by roughly a third through a different mechanism, which is why they stack. Beta-blockers are a pillar of heart-failure therapy, not of kidney protection — a common mix-up because "four pillars" is used in both fields.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO CKD guideline 2024 — 3.6.3–3.6.5; 3.7.1–3.7.3
• Kerendia US prescribing information — 2.1–2.3, CKD associated with T2D dosing table

Question · Answer and explanation

Objective: ckd-06

Diabetes damages the glomerulus (the filter) slowly and symmetrically: protein leaks, the filter does not bleed, and the decline is measured in a few mL/min a year. Retinopathy is the same small-vessel disease seen in the one organ you can look into, so its presence supports diabetes as the cause. Red-cell casts mean red cells were inside the tubules — a glomerulonephritis, which is a different disease and a same-week referral. The other atypical features to know: no retinopathy at all after a long diabetes duration, a rapid fall in eGFR, or heavy proteinuria appearing within a few years of diagnosis.

Clinical application or calculation based on the cited principles; faculty review pending.

• ADA Standards of Care in Diabetes2026: CKD and risk management — Diagnosis of CKD in people with diabetes, pS248
• KDIGO CKD guideline2024 — 1.1.4.1; Table6 and Figure8, pS174

Question · Answer and explanation

Objective: ckd-12, structural-23, structural-24

He already has pillar one — a maximally dosed ARB. Pillar two is an SGLT2 inhibitor, which KDIGO 2024 recommends for type 2 diabetes with CKD down to an eGFR of 20 regardless of glucose control; empagliflozin and dapagliflozin are both 10 mg daily with no renal dose change. He is on twice the metformin his eGFR allows (Q2), so that is fixed in the same visit — 500 mg twice daily. The ARB stays: hyperkalemia is managed around RAAS blockade, not by abandoning it. A BMP at 2 weeks is the monitoring that makes the plan safe.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO CKD guideline 2024 — 3.6.3–3.6.5; 3.7.1–3.7.3
• Metformin US prescribing information — 2.4–2.5

Question · Answer and explanation

Objective: aki-14, htn-cardiorenal-09

An SGLT2 inhibitor leaves more sodium in the tubule, the macula densa — the sensor cells where the tubule passes back beside its own glomerulus — senses it and constricts the afferent arteriole, and the pressure inside the glomerulus falls. Less pressure means less filtration right now — an eGFR dip of about 3–5 mL/min, a creatinine rise of 10–15 % — and less scarring over years. The dip appears within days, plateaus by 4–8 weeks, and reverses if the drug is stopped. The same logic applies to an ARB (its dip is efferent dilation, up to 30 %). The rule to carry: a creatinine rise of 30 % or less that stabilizes is expected; a rise above 30 %, a rise that continues to climb, or a potassium of 5.5 mEq/L or more is the signal to stop and look — for volume depletion, an NSAID, or renal artery stenosis. His 16 % is inside the line; the recheck shows whether it settles. His potassium is not, and that is Q7.

Source-supported decision rule; faculty review pending.

• KDIGO CKD guideline 2024 — 3.6.3–3.6.5; 3.7.1–3.7.3

Question · Answer and explanation

Objective: ckd-17, lytes-14

Remove the new potassium-chloride salt and NSAID and reassess kidney function, potassium trend, intake and volume status. Repeat BMP within 48–72 hours; UKKA Guideline 1.2.1 recommends repeating unexpected K 5.5–5.9 within three days. A normal ECG does not establish safety or exclude severe hyperkalemia. Outpatient management here depends on clinical stability, a reliable follow-up plan and no rapid rise; worsening symptoms, kidney function or potassium require urgent reassessment. Manage correctable hyperkalemia where possible so beneficial RAAS treatment can continue.

Source-supported decision rule; faculty review pending.

• UKKA hyperkalemia guideline July 2026 — 1.2.1–1.2.3
• KDIGO CKD guideline 2024 — 3.6.3–3.6.5; 3.7.1–3.7.3

Question · Answer and explanation

Objective: ckd-13, htn-cardiorenal-24

Finerenone is a nonsteroidal mineralocorticoid receptor antagonist: it blocks aldosterone at the collecting duct, so it raises potassium by design. The label says do not start it if potassium is above 5.0; at 4.8–5.0 start with extra monitoring; eGFR must be 25 or more (10 mg daily for eGFR 25 to under 60); check potassium at 4 weeks; hold if it exceeds 5.5. Today he fails the entry rule, so the third pillar waits for the recheck. The fourth pillar does not depend on potassium: a GLP-1 receptor agonist (semaglutide 0.25 mg weekly, titrated slowly) lowers glucose, weight, cardiovascular events and — in the FLOW trial — kidney events in people like him. Start low for the nausea, and warn him that vomiting and poor intake are a sick day (Part 3).

Source-supported decision rule; faculty review pending.

• Kerendia US prescribing information — 2.1–2.3, CKD associated with T2D dosing table

Question · Answer and explanation

Objective: aki-14

Improvement toward baseline while the SGLT2 inhibitor continues makes a sustained toxic injury caused by that drug less likely. It is compatible with an early hemodynamic change plus removal of NSAID and potassium-related contributors. It does not prove that no kidney injury occurred: mixed and recovering AKI remain possible. Continue follow-up using symptoms, volume status, serial kidney function and potassium. The preferred formative direction is much less likely; a justified less-likely answer is acceptable.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO CKD guideline 2024 — 3.6.3–3.6.5; 3.7.1–3.7.3
• KDIGO AKI guideline2012 — 2.3, printedp27; 2.5 Table13, p35

Question · Answer and explanation

Objective: aki-27, aki-15

Outpatient creatinine-bump triage runs on four things: the potassium, the symptoms, the urine output and the trajectory. A 48–72-hour recheck is for the patient who is eating and drinking, has a potassium below 5.5, is making urine and whose creatinine rise is small and plausibly hemodynamic. He fails all four — potassium 5.9 and climbing, symptomatic orthostasis, oliguria, a 45 % rise in days — and he is on a drug (empagliflozin) that can turn this exact story into euglycemic ketoacidosis. Same-day means IV fluid with reassessment, a repeat potassium within hours on a monitor, calcium only if the ECG changes, a venous gas, and every SADMANS drug held. A normal ECG at 5.9 is allowed and is not reassurance about the next six hours.

Clinical application or calculation based on the cited principles; faculty review pending.

• UKKA hyperkalemia guideline July 2026 — 1.2.1–1.2.3

Question · Answer and explanation

Objective: ckd-20, htn-cardiorenal-25, structural-23

There is no guideline-mandated ARB-first, SGLT2-next, metformin-last sequence. Confirm that volume depletion and AKI are resolving, review potassium and the creatinine trend, and restore indicated treatment with a written follow-up plan. The SGLT2 inhibitor requires adequate intake and no ongoing ketosis risk. Metformin requires recovered, stable kidney function with eGFR at least 30 and an appropriate reduced dose here. A staged restart can help attribute recurrent changes, but the order is individualized.

Clinical application or calculation based on the cited principles; faculty review pending.

• Metformin US prescribing information — 2.4–2.5
• KDIGO CKD guideline 2024 — 3.6.3–3.6.5; 3.7.1–3.7.3

Question · Answer and explanation

Objective: lytes-01

A raised JVP supports elevated right-sided filling pressure and, among these choices, is the strongest bedside congestion clue. Interpret it with symptoms, lungs, edema, weight and perfusion. It does not prove total-body volume by itself, and hepatojugular reflux adds support rather than absolute confirmation.

Clinical application or calculation based on the cited principles; faculty review pending.

• ESC guideline for the management of heart failure2026 — 5.1 Table7; 6.1.3.1; RecommendationTable5; 7.4.2; 7.5.4

Question · Answer and explanation

Objective: htn-cardiorenal-22

The four classes with outcome evidence in HFrEF are a RAAS strategy (sacubitril-valsartan, or an ACEi/ARB when ARNI is not feasible), one of three beta-blockers (carvedilol, metoprolol succinate, bisoprolol), a steroidal MRA (spironolactone or eplerenone) and an SGLT2 inhibitor (dapagliflozin or empagliflozin). All four are started early at tolerated doses rather than maximizing one first, and the monitoring labs are the BMP and potassium.

Source-supported decision rule; faculty review pending.

• ESC heart failure guideline2021 — 11.3.3 Diuretics; Key messages
• ESC guideline for the management of heart failure2026 — 5.1 Table7; 6.1.3.1; RecommendationTable5; 7.4.2; 7.5.4

Question · Answer and explanation

Objective: structural-20

In a kidney that is already under-perfused (heart failure, diuretics, volume depletion, cirrhosis), prostaglandins keep the afferent arteriole open. NSAIDs inhibit cyclooxygenase, prostaglandin production falls, the afferent arteriole constricts, and filtration pressure drops — a hemodynamic (functional) AKI with a bland urine. Add a RAAS blocker, which prevents the efferent arteriole from compensating, and a diuretic, and you have the "triple whammy."

Clinical application or calculation based on the cited principles; faculty review pending.

• Ibuprofen US prescribing information — Warnings: Renal effects

Question · Answer and explanation

Objective: aki-19, htn-cardiorenal-19

His weight gain, raised JVP and edema support substantial congestion despite the low sodium. Raised venous pressure can contribute to kidney dysfunction, while effective arterial filling can be low in the same patient. Low forward flow and other causes can coexist. A BUN:creatinine ratio of 20 alone cannot diagnose volume depletion or justify a saline bolus; reassess congestion and perfusion together.

Clinical application or calculation based on the cited principles; faculty review pending.

• Importance of venous congestion for worsening renal function in advanced decompensated heart failure2009 — Abstract: Methods and Results
• ESC guideline for the management of heart failure2026 — 5.1 Table7; 6.1.3.1; RecommendationTable5; 7.4.2; 7.5.4

Question · Answer and explanation

Objective: lytes-07

Edema, high JVP and a low urine sodium with a concentrated urine = hypervolemic hyponatremia, and it is hypotonic: effective osmolality = 2 × 127 + 148/18 = 262 mOsm/kg, because urea crosses cell membranes and is not counted — the measured 283 is misleading. The heart cannot fill the arteries well, the body reads "low effective circulating volume," antidiuretic hormone (ADH) stays on, and water is retained out of proportion to salt. The treatment is the underlying disease: restrict free water and remove salt and water together with a loop diuretic. Expect a slow rise (a few mEq/L a day); the correction ceiling of 8 mEq/L in 24 h still applies if the sodium starts to move fast.

Clinical application or calculation based on the cited principles; faculty review pending.

• European hyponatraemia guideline: official short version 2014 — 2.2–2.3, pp7–9; Tables3–4, pp16–17; 3.4

Question · Answer and explanation

Objective: htn-cardiorenal-20

The initial total daily IV loop regimen can reasonably be 1–2 times the previous total daily oral dose (ESC 2021 §11.3.3); individual response determines escalation. Here urine output is 90 mL/h and urine sodium 28, below commonly used early response goals of >100–150 mL/h or >50–70 mmol/L. Double the IV dose and reassess rather than labeling the starting regimen intrinsically wrong. Integrate weight, net balance, blood pressure and symptoms with these surrogate targets.

Source-supported decision rule; faculty review pending.

• ESC heart failure guideline2021 — 11.3.3 Diuretics; Key messages

Question · Answer and explanation

Objective: htn-cardiorenal-20, aki-19

Persistent congestion and little weight loss favor continuing monitored decongestion while stopping ibuprofen and checking perfusion and electrolytes. Modest creatinine rises can accompany effective decongestion without structural injury, but no universal 30% rule proves that a rise is benign. Intrinsic injury can coexist. Reassess hypotension, urine output, exposures and the trend; monitor potassium more promptly when it is rising and obtain BMP and magnesium at least twice daily during intensive combination diuresis.

Clinical application or calculation based on the cited principles; faculty review pending.

• ESC heart failure guideline2021 — 11.3.3 Diuretics; Key messages

Question · Answer and explanation

Objective: lytes-01, aki-19

Persistent weight excess and a raised JVP make simple whole-body volume depletion from over-diuresis less likely. They support continuing a careful assessment for residual congestion. They do not exclude impaired arterial perfusion, excessive plasma-volume reduction during diuresis or another AKI mechanism. The decision must also use blood pressure, symptoms, urine output and the creatinine trajectory. A is the preferred formative direction; a well-justified adjacent response is acceptable.

Clinical application or calculation based on the cited principles; faculty review pending.

• Importance of venous congestion for worsening renal function in advanced decompensated heart failure2009 — Abstract: Methods and Results
• KDIGO AKI guideline2012 — 2.3, printedp27; 2.5 Table13, p35
• ESC guideline for the management of heart failure2026 — 5.1 Table7; 6.1.3.1; RecommendationTable5; 7.4.2; 7.5.4

Question · Answer and explanation

Objective: htn-cardiorenal-21, lytes-27

Despite a high IV loop dose, he remains congested and now has urine sodium 44 and only 75 mL/h over two hours. Discuss adding a thiazide-like diuretic with the supervising heart-failure or nephrology team. Combination treatment can produce large electrolyte and volume changes, so follow weight, net balance, blood pressure, BMP and magnesium at least twice daily initially, with earlier potassium reassessment when indicated. Metolazone is one acceptable option; acetazolamide is another selected by the treating team, and there is no universally mandatory ladder.

Source-supported decision rule; faculty review pending.

• ESC heart failure guideline2021 — 11.3.3 Diuretics; Key messages
• ESC guideline for the management of heart failure2026 — 5.1 Table7; 6.1.3.1; RecommendationTable5; 7.4.2; 7.5.4

Question · Answer and explanation

Objective: ckd-17, htn-cardiorenal-23

K 5.6 needs active evaluation, treatment and prompt remeasurement; a normal ECG does not exclude danger. Stop potassium-raising contributors and keep the steroidal MRA held because eGFR is below 30 and potassium is elevated. Continue or adjust ARNI according to perfusion, potassium response and renal trajectory, using a binder when appropriate. Continue empagliflozin only if he is stable, eating and without ketosis risk; withhold during critical illness or prolonged fasting. Preserve the beta-blocker when possible, but shock, marked bradycardia or symptomatic hypotension can require adjustment. Drug benefit does not replace bedside reassessment.

Clinical application or calculation based on the cited principles; faculty review pending.

• UKKA hyperkalemia guideline July 2026 — 1.2.1–1.2.3
• KDIGO CKD guideline 2024 — 3.6.3–3.6.5; 3.7.1–3.7.3

Question · Answer and explanation

Objective: htn-cardiorenal-22, htn-cardiorenal-23

"Renalism" is the reflex to deny kidney patients the heart therapies everyone else gets — because the trials "didn't include them," because the creatinine might move, because "he'll be on dialysis anyway" — and the CKD patient is the one with the most to lose. Cardiovascular death risk climbs steeply as eGFR falls and albuminuria rises — several-fold at G4 A3, 10–20 times once on dialysis — and most CKD patients die of their hearts before they ever reach dialysis, so the four pillars protect both organs. The rule is to adjust and monitor, not eliminate: SGLT2 inhibitor — start at eGFR ≥20; once started, continue even below 20 until dialysis unless not tolerated (KDIGO 2024), and the eGFR dip it causes is protective, not injury; the ARNI is continued in advanced CKD with potassium and creatinine monitoring; the beta-blocker needs no renal adjustment; only the steroidal MRA fails the numbers (eGFR >30, K⁺ <5.0) and stays off. CKD is also an atherosclerotic cardiovascular disease (ASCVD) risk equivalent — his statin stays, and his LDL of 68 says it is doing its job.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO CKD guideline 2024 — 3.6.3–3.6.5; 3.7.1–3.7.3
• ESC heart failure guideline2021 — 11.3.3 Diuretics; Key messages

Question · Answer and explanation

Objective: glom-01

Nitrite is not made by the body. Gut-type bacteria (E. coli, Klebsiella, Proteus) carry an enzyme, nitrate reductase, that converts dietary nitrate in the urine into nitrite — and that takes about 4 hours of bladder dwell time. A first-morning void is the right specimen; a patient voiding every hour, on a diuretic, can have a florid infection with a blank nitrite pad. Some organisms, including Enterococcus, commonly yield a negative nitrite result. Do not treat nitrite behavior as a perfectly sensitive organism-identification test.

Clinical application or calculation based on the cited principles; faculty review pending.

• Siemens urinalysis reagent-strip instructions for use — Nitrite performance characteristics and limitations, p1

Question · Answer and explanation

Objective: glom-02, aki-06

Casts form inside renal tubules from a protein matrix; incorporated white cells therefore locate the inflammatory process to the kidney. Pyelonephritis, interstitial nephritis and some glomerulonephritides can produce white-cell casts. The cast does not identify one of these causes by itself.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO AKI guideline2012 — 2.3, printedp27; 2.5 Table13, p35

Question · Answer and explanation

Objective: lytes-06, structural-25

Thiazides block salt reabsorption in the distal tubule, the segment that dilutes urine, so the kidney loses the ability to excrete free water while still losing salt. The patients who get into trouble are older women with low body weight, and the drop happens within the first weeks of the drug . Add an SSRI and the risk climbs further. Age, low weight and recent start — option B has all three.

Clinical application or calculation based on the cited principles; faculty review pending.

• Risk factors for thiazide-induced hyponatraemia2003 — Abstract: Results and Conclusions
• Hydrochlorothiazide US prescribing information — Precautions: Fluid and electrolyte balance

Question · Answer and explanation

Objective: structural-04, glom-02

Confusion without urinary symptoms or systemic signs is not an indication to diagnose or treat UTI or routinely screen for bacteriuria. This poorly collected bag specimen adds little diagnostic value. Follow IDSA 2019 §§IV–V: assess other causes of delirium and observe rather than prescribe an antibiotic. If new localizing or systemic findings create a clinical reason to test, obtain an appropriate specimen; a straight catheter is not routinely required simply to replace an incidental abnormal urinalysis.

Source-supported decision rule; faculty review pending.

• IDSA asymptomatic bacteriuria guideline2019 — IV, V.1–V.2; III; XIII

Question · Answer and explanation

Objective: lytes-01, lytes-06

Hyponatremia is too much water relative to salt, and the first question is always volume status at the bedside — she is hypovolemic (orthostatic drop, heart-rate rise of 20, dry mucosa, flat neck veins, 2.5 kg lost). The thiazide is the cause: it wrecks urinary dilution and wastes salt in exactly her demographic — older woman, 52 kg, started within weeks — so the treatment is to stop the drug and replace volume with isotonic saline, slowly. The trap is what happens next: once the drug wears off and volume is restored the kidney dumps free water and the sodium can shoot up, which is why the recheck is every 4–6 hours and why the ceiling is no more than 8 mEq/L in the first 24 hours in a high-risk patient like her (elderly, malnourished; never more than 10), to avoid osmotic demyelination, a brain injury from correcting too fast .

Clinical application or calculation based on the cited principles; faculty review pending.

• Society for Endocrinology emergency hyponatraemia guidance 2022 — Treatment recommendation 1(a–d), Figure1

Question · Answer and explanation

Objective: ckd-18, structural-18

Her calculated Cockcroft–Gault clearance is about 25 mL/min. Gabapentin accumulation can produce somnolence, myoclonus and falls, so withhold it during assessment of suspected toxicity and review the indication. The label gives 200–700 mg once daily at CrCl >15–29, 100–300 mg/day at 15, and proportionate reduction below 15. A frail patient may need less; the label range is not a target to titrate toward. Reassess alertness and kidney function before a cautious restart.

Source-supported decision rule; faculty review pending.

• Gabapentin US prescribing information — 2.3 Table1 renal dosing; withdrawal precautions

Question · Answer and explanation

Objective: structural-04

The finding's meaning depends on a circumstance you must notice — which specimen: the bag urinalysis never counted (its leukocyte esterase and bacteria reported her skin, not her bladder), so the catheter specimen is the first real look, and it is quiet on every axis — no pyuria (fewer than 5 WBC/hpf), no bacteria, both infection pads negative. Negative leukocyte esterase and nitrite is the dipstick's one strong move, a rule-out , while in older adults a positive pad is nearly useless as a rule-in (specificity for infection about 39% in symptomatic older adults ). A negative nitrite alone would not reassure you (short dwell time on a diuretic; Enterococcus and staphylococci never turn the pad), but absent pyuria is different: in institutionalized older women even asymptomatic bacteriuria carries pyuria about 90% of the time (review §3.3), and treating "delirium plus bacteriuria" with an antibiotic has not been shown to help . "Much less likely" — stop looking there and treat what you found: sodium 127, gabapentin far above her dose band, an anticholinergic, dehydration.

Clinical application or calculation based on the cited principles; faculty review pending.

• IDSA asymptomatic bacteriuria guideline2019 — IV, V.1–V.2; III; XIII

Question · Answer and explanation

Objective: structural-04

Mixed low-count growth from a poorly collected bag specimen, no urinary or systemic symptoms and an uninflamed catheter specimen do not support UTI. Do not give antibiotics or repeat cultures reflexively. Colony-count thresholds depend on symptoms and collection method: clinically meaningful infection can occur below 100,000 CFU/mL, and even high counts without compatible symptoms may be asymptomatic bacteriuria.

Source-supported decision rule; faculty review pending.

• IDSA asymptomatic bacteriuria guideline2019 — IV, V.1–V.2; III; XIII

Question · Answer and explanation

Objective: aki-27, structural-25

An unexpected creatinine rise gets the same five moves every time — repeat the BMP, review the medications and the intake, look at the urine, scan the bladder, then choose same-day care versus a 48–72-hour recheck from the potassium, the symptoms, the urine output and the trajectory. Her pattern is prerenal (poor intake, orthostasis, BUN:creatinine 22:1, bland sediment with hyaline casts, no retention on the bladder scan), and on its own a rise of this size in a patient who is drinking, making urine and has no hyperkalemia would be a 48–72-hour outpatient recheck. She is not that patient: she cannot drink, she is confused, and her sodium needs a check every few hours — the whole patient decides the disposition, not the 1.9. Same-day orders: cautious isotonic saline (see Q5), hold metformin and lisinopril, stop hydrochlorothiazide, gabapentin and diphenhydramine, and print no eGFR while the creatinine is moving.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO AKI guideline 2012 — 2.1.1–2.1.2; Table2, printedp19

Question · Answer and explanation

Objective: structural-05

Fever, flank tenderness and inflammatory urine support pyelonephritis; delirium, poor intake and possible AKI favor hospital care. Obtain urine and, when indicated, blood cultures before antibiotics if this does not delay treatment of sepsis. Ceftriaxone is a reasonable initial option depending on local resistance and prior cultures; generally no adjustment is needed for isolated renal impairment at usual doses. Evaluate promptly for obstruction; ultrasound is useful for hydronephrosis, while CT may be needed for stones, abscess or persistent complicated infection. Select and reassess all other drug doses using the current renal trajectory and pharmacy advice, not an old baseline alone.

Clinical application or calculation based on the cited principles; faculty review pending.

• IDSA complicated urinary tract infection guideline2025 — Question1, recommendationI(a), four-step empiric-antibiotic selection

Question · Answer and explanation

Objective: ckd-18, structural-25

The thiazide caused a sodium of 127 within four weeks in exactly the patient the risk tables describe — an older woman of low body weight — and rechallenge reproduces it, so it is replaced with a different class (a low-dose dihydropyridine such as amlodipine is a common choice at 84) and goes on her allergy-and-intolerance list. The rest of the list is a restart-when-safe list, not a stop list: lisinopril comes back now that she is euvolemic with the creatinine at baseline, because her albuminuria (UACR 210 mg/g) is the indication and the ACE inhibitor protects the kidney; metformin comes back at 500 mg twice daily, the capped dose for eGFR 30–45, because it was held for the acute illness, not stopped for her CKD; the statin was never the problem. Gabapentin and diphenhydramine are handled separately at discharge — see the Resolution.

Clinical application or calculation based on the cited principles; faculty review pending.

• Gabapentin US prescribing information — 2.3 Table1 renal dosing; withdrawal precautions
• Metformin US prescribing information — 2.4–2.5

Question · Answer and explanation

Objective: glom-06

Red cells that squeeze through an inflamed glomerulus come out deformed; his are uniform discs, with no protein, no casts, and clots at the end of the stream — a pattern favoring nonglomerular urinary-tract bleeding; an upper-tract source remains possible. The question is no longer "which glomerulonephritis" but "which part of the urinary tract is bleeding, and is it a cancer." The AUA/SUFU microhematuria guideline's high-risk category is age ≥60, more than 30 pack-years, more than 25 RBC/hpf, or any gross hematuria — he qualifies on the pack-years and the gross hematuria alone. High risk means cystoscopy for the bladder and CT urography for the upper tract.

Source-supported decision rule; faculty review pending.

• AUA/SUFU Microhematuria guideline2025 — Guideline15; high-risk evaluation

Question · Answer and explanation

Objective: glom-12, htn-cardiorenal-17

Palpable purpura, joint pain, abdominal pain and hematuria/proteinuria suggest IgA vasculitis with kidney involvement. In the AAP Table 4 row for a 9-year-old boy at the 50th height percentile (136.3 cm), the 95th percentile is 115/76 and the 95th percentile plus 12 mmHg is 127/88. His repeated 128/84 is therefore in the stage 2 range by systolic pressure. The AAP table reproduced by Connecticut Children's, Appendix G, page 2 supplies the numerical row. This is a BP category at this visit, not proof of chronic primary hypertension. Active kidney findings warrant prompt pediatric assessment and nephrology advice; severe symptoms or marked pressure elevation require emergency evaluation.

Clinical application or calculation based on the cited principles; faculty review pending.

• AAP 2017 pediatric blood pressure Table4, institutional reproduction — AppendixG, PDFpage2, boys age9/50th-height column
• IPNA clinical practice recommendations for IgA nephropathy and IgA vasculitis nephritis2025 — Introduction; Clinical presentation and diagnosis

Question · Answer and explanation

Objective: glom-02

A cast is a cylinder molded inside a kidney tubule around a protein core (uromodulin, the Tamm-Horsfall protein), so whatever is trapped inside came from the kidney — never the bladder, prostate or vagina — and names the injured compartment. Ischemia after shock kills tubular cells; they slough into the lumen and degrade into coarse granular debris that looks like mud. Muddy brown casts with tubular cells, a urine the kidney can no longer concentrate (specific gravity near 1.010) and oliguria three days after vasopressors is acute tubular necrosis.

Clinical application or calculation based on the cited principles; faculty review pending.

• Diagnostic value of urine microscopy for differential diagnosis of AKI2008 — Introduction; Methods; diagnostic sediment results

Question · Answer and explanation

Objective: glom-03, glom-06

A dipstick heme pad turns positive for intact red cells, free hemoglobin from hemolysis and myoglobin from muscle breakdown alike; it cannot tell them apart and it cannot see shape. Hematuria is a microscope word — the AUA/SUFU guideline defines microhematuria as three or more red cells per high-power field on a properly collected specimen, confirmed before a positive pad triggers any evaluation. The same drop of urine then answers the second question: misshapen (dysmorphic) cells, ring forms with blebs (acanthocytes) or cells packed into a cast came through a glomerulus, and the UPCR puts a number on the protein pad.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2021 glomerular disease general-principles key takeaways — Points1–4,6,8

Question · Answer and explanation

Objective: glom-12, glom-13

Two diseases, two clocks. In IgA nephropathy the abnormal IgA is already sitting in the mesangium, so a mucosal infection lights it up within a day or two — cola urine while the throat still hurts, peaking in young adults. Post-infectious GN has to wait for an antibody response, immune-complex formation and deposition: 1–3 weeks after a strep throat, 3–6 weeks after impetigo. A sore throat on Sunday and dark urine on Tuesday is the wrong tempo for post-streptococcal disease, and her negative rapid strep fits — most synpharyngitic flares follow a viral pharyngitis, not strep.

Clinical application or calculation based on the cited principles; faculty review pending.

• IPNA clinical practice recommendations for IgA nephropathy and IgA vasculitis nephritis2025 — Introduction; Clinical presentation and diagnosis
• CDC clinical guidance for post-streptococcal glomerulonephritis — Clinical features; latency; laboratory findings

Question · Answer and explanation

Objective: glom-17, glom-23

Complement is the first sort in a nephritic sediment: both low → classical pathway (lupus, cryoglobulinemia — antibodies that clump in the cold, usually from hepatitis C — endocarditis, MPGN); low C3 with normal C4 → alternative pathway (post-infectious GN, C3 glomerulopathy); both normal → IgA nephropathy, ANCA vasculitis and anti-GBM disease, which do not consume complement. Normal complement plus synpharyngitic timing in a 19-year-old makes IgA the working diagnosis. Complement sorts the probability; it does not replace the panel — ANA goes with every nephritic sediment, ANCA and anti-GBM with any that could be RPGN. The plan follows the sediment, not the creatinine: RBC casts with proteinuria earn a phone call today, not a referral form, and the NSAID stops.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO Lupus Nephritis guideline2024 — 10.1.1 Figure1, pS15/S23
• CDC clinical guidance for post-streptococcal glomerulonephritis — Clinical features; latency; laboratory findings
• KDIGO 2021 anti-GBM glomerulonephritis key takeaways — Figure1 diagnosis and treatment; key points

Question · Answer and explanation

Objective: glom-15, aki-01, aki-02

The creatinine ratio is 2.4, which fits stage 2 if the increase is known or reasonably presumed to have occurred within seven days. Her acute illness and active nephritic sediment make acute worsening concerning, but the three-week-old baseline alone cannot establish that interval. Document presumed AKI, obtain the intervening trend urgently and treat possible rapidly progressive GN without waiting for perfect staging. A changing creatinine also makes the printed steady-state eGFR unreliable.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO AKI guideline 2012 — 2.1.1–2.1.2; Table2, printedp19
• KDIGO CKD guideline 2024 — 1.3 GFR evaluation, pS175–S180; errors with non-steady state

Question · Answer and explanation

Objective: glom-15, glom-17, glom-23

RPGN has three immune causes and one stat panel finds all three: ANCA (PR3 and MPO) for the pauci-immune vasculitides — pauci-immune means few or no antibody deposits on biopsy, which is why the ANCA pattern needs a blood test to find — anti-GBM antibody for anti-GBM disease, and ANA with anti-dsDNA and both complements for lupus. Blood cultures ride along in anyone febrile, because endocarditis causes a low-complement GN that will fool you; the chest film looks for pulmonary hemorrhage; the ultrasound confirms two normal-sized, unobstructed kidneys before anyone considers a needle. All of it leaves the clinic within the hour, and "RPGN" said aloud to a nephrologist buys a same-day evaluation. Do not wait for the biopsy to send the serology, and do not wait for the serology to make the call.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO Lupus Nephritis guideline2024 — 10.1.1 Figure1, pS15/S23

Question · Answer and explanation

Objective: glom-14, glom-17

IgA nephropathy does not consume serum complement — it sits in the normal-complement column with ANCA vasculitis and anti-GBM disease, which is why her normal C3 and C4 three weeks ago supported it. Both C3 and C4 low is the classical-pathway fingerprint of circulating immune complexes — lupus nephritis first, then cryoglobulinemia (check hepatitis C), endocarditis (hence the cultures) and MPGN — so the hypothesis moves a long way: "much less likely," not "excluded," because serology is a probability and nephrology still has to see tissue. The circumstance that gives the finding its meaning is that it is both complements; C3 42 with a normal C4 would be the alternative pathway (post-infectious GN, C3 glomerulopathy) and a different move — read the C4 before you move. None of the alternatives fits a 19-year-old woman with a malar rash, oral ulcer, arthritis and three low cell lines, and the panel below confirms it: this is lupus nephritis presenting as RPGN, and the first complements were not wrong, they were early.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO Lupus Nephritis guideline2024 — 10.1.1 Figure1, pS15/S23

Question · Answer and explanation

Objective: aki-22, aki-24

Her potassium 5.6 with worsening AKI needs close reassessment, removal of contributors and nephrology involvement. A normal ECG does not exclude hyperkalemic arrhythmic risk, and specific ECG patterns cannot be assigned reliable potassium ranges. Give IV calcium for toxic hyperkalemic ECG changes; severe potassium elevation needs urgent potassium-lowering treatment even without ECG changes. Empiric calcium when an ECG or monitoring is unavailable is a protocol-dependent emergency decision, not a universal potassium-only rule. Calcium does not remove potassium. Stop naproxen and avoid potassium supplementation; repeat potassium and ECG in 2–4 hours, sooner for deterioration. There is no current refractory electrolyte/acid-base disorder, pulmonary edema, relevant dialyzable toxin or uremic complication establishing an immediate dialysis indication. Continue reassessing the whole clinical picture.

Clinical application or calculation based on the cited principles; faculty review pending.

• UKKA hyperkalemia guideline July 2026 — 14.1–14.2, 15.2–15.3, 16.2a–b
• KDIGO AKI guideline 2012 — 5.1.1–5.1.2

Question · Answer and explanation

Objective: htn-cardiorenal-08

Treat the hypertension while arranging urgent nephrology evaluation and biopsy. Amlodipine is a reasonable temporary choice while K is 5.6 and kidney function is deteriorating. Biopsy blood-pressure thresholds are center-specific; uncontrolled hypertension increases bleeding risk and requires management. Defer initiation of ACEi/ARB until potassium, kidney trajectory and reproductive precautions have been reviewed. The pregnancy test is already negative. Immunosuppression is the specialist team's decision; in some rapidly progressive syndromes, treatment should not wait for biopsy results.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO Lupus Nephritis guideline2024 — 10.1.1 Figure1, pS15/S23
• KDIGO CKD guideline 2024 — 3.6.3–3.6.5; 3.7.1–3.7.3

Question · Answer and explanation

Objective: glom-16

Pulmonary hemorrhage with rapidly progressive glomerulonephritis is an emergency. The strongly positive anti-GBM result identifies the leading diagnosis; the lung–kidney pattern alone cannot distinguish anti-GBM disease from ANCA-associated vasculitis. KDIGO advises urgent serology and biopsy, and treatment without delay when anti-GBM disease is suspected. Specialist-directed plasma exchange and immunosuppression may begin before final confirmation; the student's task is recognition and immediate escalation.

Source-supported decision rule; faculty review pending.

• KDIGO 2021 anti-GBM glomerulonephritis key takeaways — Figure1 diagnosis and treatment; key points

Question · Answer and explanation

Objective: glom-04

The KDIGO albuminuria categories are A1 below 30 mg/g, A2 30–300 mg/g, A3 above 300 mg/g. A UACR of 420 mg/g is A3. Nephrotic range is a different and much higher bar — more than 3.5 g of protein per gram of creatinine on a UPCR, which corresponds to a UACR of roughly 2,200 mg/g or more (KDIGO). A3 means risk and the protective drugs; nephrotic range means a syndrome with its own differential.

Source-supported decision rule; faculty review pending.

• KDIGO CKD guideline 2024 — Tables1–3, pS137; 1.1 chronicity/albuminuria evaluation

Question · Answer and explanation

Objective: glom-07

Heavy proteinuria with hypoalbuminemia and edema defines the nephrotic syndrome; hyperlipidemia and lipiduria support the pattern. The bland, fatty sediment in C fits. A nephritic pattern emphasizes glomerular bleeding and inflammation, often with RBC casts, hypertension and impaired filtration. These are patterns rather than mutually exclusive diseases: inflammatory GN can cause nephrotic-range proteinuria, and nephrotic disease can include hematuria.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2021 glomerular disease general-principles key takeaways — Points1–4,6,8
• KDIGO CKD guideline 2024 — Tables1–3, pS137; 1.1 chronicity/albuminuria evaluation

Question · Answer and explanation

Objective: structural-23

Metformin is cleared by the kidney and accumulates as GFR falls; the rare but real danger is lactic acidosis. The rules: do not start below 45, reduce between 30 and 45, stop below 30, and hold during dehydrating illness or AKI. For IV iodinated contrast, the ACR approach permits continuation with stable eGFR ≥30 and no AKI; the drug label and some local policies are stricter. Certain arterial catheter procedures also require holding.

Clinical application or calculation based on the cited principles; faculty review pending.

• Metformin US prescribing information — 2.4–2.5

Question · Answer and explanation

Objective: glom-05, ckd-06

Fever, hard exercise, stress and seizures push protein into the urine for a day or two — transient proteinuria — and standing up all day does the same in some tall, thin young people — orthostatic proteinuria, which is benign and needs no workup once a first-morning sample is clean. A kidney label is a lifelong label; it rests on a first-morning sample collected when the patient is well, and chronic kidney disease requires the abnormality to persist for more than three months. Her repeat first-morning UACR two weeks later is 380 mg/g, and a third at three months is 350 mg/g. Now she is honestly G2 A3.

Source-supported decision rule; faculty review pending.

• KDIGO CKD guideline 2024 — Tables1–3, pS137; 1.1 chronicity/albuminuria evaluation

Question · Answer and explanation

Objective: glom-22, ckd-12

Both drugs lower the pressure inside the glomerulus — that is the point — and a lower filtration pressure means a lower eGFR for as long as the drug is on board. The expected drop is 10–30 % within the first weeks; then it plateaus, and over years the slope of decline is flatter than it would have been. Accept a creatinine rise of up to 30 %, recheck in two weeks, continue, and titrate lisinopril to 40 mg at six weeks as planned. A rise above 30 %, or one that keeps climbing, is the signal to look for volume depletion, an NSAID, or renal artery stenosis.

Source-supported decision rule; faculty review pending.

• KDIGO CKD guideline 2024 — 3.6.3–3.6.5; 3.7.1–3.7.3

Question · Answer and explanation

Objective: glom-11, glom-18, glom-24

Diabetic kidney disease is the leading cause of nephrotic syndrome in a diabetic, but it is a diagnosis you earn by checking that nothing else fits. The clues that say "maybe not diabetes" are: nephrotic-range proteinuria that arrives suddenly or with a short diabetes duration, hematuria or an active sediment, no retinopathy, a rapid GFR decline, and positive serologies. She has one soft clue (a sudden jump to nephrotic range), one equivocal one (trace blood, but isomorphic and castless), one unknown (the eye exam), and one real confounder — an NSAID. NSAIDs cause minimal change disease and membranous nephropathy, not only interstitial nephritis; they also raise blood pressure and potassium and blunt every diuretic. Stop it today. Every adult with new nephrotic syndrome gets the secondary-cause screen — glucose and A1c, HIV, hepatitis B and C, ANA with complements (C3 and C4), serum protein electrophoresis (SPEP) with serum free light chains (especially over 50 or when dipstick protein is lower than the UPCR suggests) — and anti-PLA2R when membranous nephropathy is suspected, without an age-40 restriction (the membranous nephropathy antibody). Nephrotic syndrome in an adult is a referral.

Clinical application or calculation based on the cited principles; faculty review pending.

• ADA Standards of Care in Diabetes2026: CKD and risk management — Diagnosis of CKD in people with diabetes, pS248
• KDIGO 2021 glomerular disease general-principles key takeaways — Points1–4,6,8

Question · Answer and explanation

Objective: glom-21

Nephrotic patients need more loop diuretic, by mouth, more often. Oral furosemide's absorption is unreliable in anyone (10–100 %) and worse when the gut wall is swollen; the drug reaches its site of action by being secreted into the tubule, and low albumin reduces that delivery. Once-daily dosing leaves 16 hours in which the kidney claws the sodium back. So: 80 mg twice daily, a sodium limit below 2 g/day (the diuretic cannot outrun a salty diet), and a target of 0.5–1 kg a day — faster than that empties the blood volume and buys an acute kidney injury, the lesson of the "resistant heart failure" patient on the website. Weight, potassium and creatinine twice a week catch both failure and overshoot. Metolazone is the step you add only when a good loop dose has plateaued, with labs at least twice weekly because the combination wastes potassium, sodium and magnesium.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2021 glomerular disease general-principles key takeaways — Points1–4,6,8

Question · Answer and explanation

Objective: glom-19

The urine carries away more than albumin. It loses antithrombin and protein S while the liver overproduces fibrinogen — so nephrotic patients clot: deep vein thrombosis, pulmonary embolism, and renal vein thrombosis (flank pain, new hematuria, a sudden creatinine jump), highest in membranous nephropathy and when albumin is below 2–2.5 g/dL. It loses immunoglobulins — so they get infections with encapsulated bacteria, which is why the pneumococcal vaccine is given now. The liver's lipoprotein surge is why the statin goes up, not away. And over-diuresis causes acute kidney injury. Whether to anticoagulate prophylactically is a weighed decision made with nephrology, balancing clot risk against bleeding; it is not a primary-care reflex.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2021 glomerular disease general-principles key takeaways — Points1–4,6,8

Question · Answer and explanation

Objective: glom-11, glom-23

Absence of diabetic retinopathy lowers confidence in DKD but does not exclude it, especially in type 2 diabetes. It does not determine the size of a probability update. Her abrupt nephrotic syndrome and NSAID exposure require nephrology assessment for a superimposed disease even with bland sediment and negative serologies. Biopsy versus an explicitly monitored short interval of observation is individualized; a bland urine and normal eye examination do not automatically justify waiting 8–12 weeks.

Clinical application or calculation based on the cited principles; faculty review pending.

• ADA Standards of Care in Diabetes2026: CKD and risk management — Diagnosis of CKD in people with diabetes, pS248
• KDIGO 2021 glomerular disease general-principles key takeaways — Points1–4,6,8

Question · Answer and explanation

Objective: ckd-13, ckd-17

Do not initiate finerenone: potassium 5.5 exceeds its initiation limit and eGFR 21 is below its recommended initiation threshold of 25. Correct reversible potassium contributors and arrange close follow-up while preserving tolerated kidney-protective treatment when safe. An established SGLT2 inhibitor need not be stopped simply for crossing eGFR 30. Continued ACE-inhibitor treatment requires monitoring and may need interruption if hyperkalemia remains uncontrolled despite treatment. Metformin should already have stopped below eGFR 30.

Source-supported decision rule; faculty review pending.

• Kerendia US prescribing information — 2.1–2.3, CKD associated with T2D dosing table
• UKKA hyperkalemia guideline July 2026 — 1.2.1–1.2.3

Question · Answer and explanation

Objective: ckd-09, ckd-22, ckd-24

KDIGO 2024 puts action thresholds on the KFRE: a 5-year risk of 3–5 % is a nephrology referral, a 2-year risk above 10 % is multidisciplinary care, and a 2-year risk above 40 % is modality education, access planning and transplant preparation. Her 2-year risk of about 41 % is past that 40 % line today, and her slope — eGFR 58 to 21 in two years, 15 within months — says the same; KDIGO 2024 and KDOQI also support kidney-replacement education, vein preservation, vascular-surgery referral and pre-emptive transplant referral at an eGFR of about 20. Education starts at G4 because every option takes months: a fistula takes months to be usable and transplant evaluation takes most of a year — so every referral goes today, and a pre-emptive living-donor transplant, before any dialysis, is the best outcome available. The options are told in plain words: in-center hemodialysis three times a week for about four hours; home hemodialysis; peritoneal dialysis through a belly catheter, usually overnight at home; transplant; and conservative kidney management — active, symptom-focused care without dialysis, which is a real option for a frail or very old patient or anyone who chooses it. The surprise question — "would I be surprised if she died in the next year?" — is answered yes, I would be surprised for a 52-year-old with no other major illness, which is why she is a transplant candidate; but the option is always named. Vein preservation starts today: no PICC, no IV, no blood pressure cuff in the non-dominant arm, because a PICC scars the very veins a fistula needs.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO CKD guideline 2024 — 2.2.1–2.2.3, pS156; Figure48; 5.4.1 and Table41
• KDOQI Vascular Access 2019 Update — 1.1–1.3, 2.1; 6.1, 6.6, 6.10

Question · Answer and explanation

Objective: ckd-22, ckd-25

On hemodialysis, fluid leaves the body three times a week; everything she drinks between sessions, and everything her 600 mL of urine does not remove, is the interdialytic gain that the machine must take off next time. A 4-kg gain means 4 L removed in four hours — which is how cramps, hypotension and a stunned heart happen — so the gain, not the dialysis, is the thing to fix. Sodium drives thirst; a 2-g sodium diet is the lever, with a fluid allowance the unit sets (typically about a liter plus her urine output). Dry weight is nephrology's number and moves with her nutrition; it is reassessed, not assumed. And residual kidney function is precious: as long as she makes urine, the loop diuretic still works, protects her from gains, and stays — it is stopped only when she is anuric.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO CKD guideline 2024 — 2.2.1–2.2.3, pS156; Figure48; 5.4.1 and Table41

Question · Answer and explanation

Objective: aki-01

AKI is a change, not a number: KDIGO 2012 defines it as a creatinine rise ≥0.3 mg/dL within 48 hours or to ≥1.5 times baseline within 7 days, or urine output below 0.5 mL/kg/h for 6 hours. The 0.3 rule gets you in the door; the stage is the ratio to baseline — stage 1 = 1.5–1.9×, stage 2 = 2.0–2.9×, stage 3 = ≥3.0× or an absolute creatinine ≥4.0 mg/dL or dialysis started. 1.9 ÷ 0.8 = 2.4 → stage 2. If the creatinine stage and the urine-output stage disagree, use the higher one.

Source-supported decision rule; faculty review pending.

• KDIGO AKI guideline 2012 — 2.1.1–2.1.2; Table2, printedp19

Question · Answer and explanation

Objective: aki-06

The sediment map the whole case runs on: hyaline casts (clear Tamm-Horsfall protein) with concentrated urine → prerenal, tubules intact and working hard; muddy brown granular casts (dead tubular cells and debris) with urine stuck at 1.010 → ATN; white-cell casts with sterile pyuria (white cells, negative culture) 1–2 weeks into an antibiotic → acute interstitial nephritis (AIN), inflammation in the tissue between the tubules; red-cell casts and dysmorphic red cells → glomerulonephritis and an urgent nephrology call. Urine eosinophils do not help with AIN — do not order them.

Clinical application or calculation based on the cited principles; faculty review pending.

• Diagnostic value of urine microscopy for differential diagnosis of AKI2008 — Introduction; Methods; diagnostic sediment results
• KDIGO AKI guideline2012 — 2.3, printedp27; 2.5 Table13, p35

Question · Answer and explanation

Objective: aki-09

A rising creatinine after several days of aminoglycoside exposure with a tubular sediment is consistent with nephrotoxic tubular injury. Stop or substitute the drug if possible, check concentrations and reassess the antimicrobial indication. Enterococcal endocarditis may require a specific synergistic regimen; do not apply a routine large-dose every-24–48-hour schedule automatically. Infectious diseases and pharmacy should select an alternative or individualized regimen.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO AKI guideline2012 — 3.8.1–3.8.4, printedpp61–63

Question · Answer and explanation

Objective: aki-03, aki-04, aki-23

Prerenal means the kidney is under-perfused but the tubules still work, and working tubules do two things when the body is dry — concentrate the urine (specific gravity above 1.020) and hold onto sodium — with a bland sediment, because hyaline casts are protein, not dead cells. Walter has the story, the exam and the urine of intact tubules — 3.5 kg lost, a 20-point systolic drop with a 20-beat rise, flat neck veins, specific gravity 1.024; a BUN:creatinine ratio of 58 ÷ 2.4 = 24 fits, because urea is reabsorbed with water when the kidney is dry and nothing else (GI bleed, steroids) is raising it. The test of prerenal physiology is not a lab but the response to fluid: a 500 mL bolus (smaller in a 79-year-old), then recheck pulse, pressure and urine output, and repeat.

Clinical application or calculation based on the cited principles; faculty review pending.

• Diagnostic value of urine microscopy for differential diagnosis of AKI2008 — Introduction; Methods; diagnostic sediment results
• KDIGO AKI guideline2012 — 2.3, printedp27; 2.5 Table13, p35

Question · Answer and explanation

Objective: aki-13, aki-15

Naproxen, lisinopril and hydrochlorothiazide are the triple whammy: the thiazide drains the tank, the ACE inhibitor removes angiotensin II's squeeze on the efferent (outflow) arteriole that holds pressure inside the glomerulus, and the NSAID removes the prostaglandins that keep the afferent (inflow) arteriole open — add diarrhea and no autoregulation is left (Lapi 2013, in the References). NSAID off first, with acetaminophen or topical diclofenac instead; the ACE inhibitor and thiazide are held while he is dry (the sick-day list), with a written plan to restart. Metformin is held in any AKI because it accumulates toward lactic acidosis, atorvastatin stays, and renally cleared gabapentin needs urgent dose reduction or holding if toxicity is suspected, with monitoring for withdrawal and seizures; the decision depends on the indication, symptoms and renal trajectory.

Clinical application or calculation based on the cited principles; faculty review pending.

• Metformin US prescribing information — 2.4–2.5
• Gabapentin US prescribing information — 2.3 Table1 renal dosing; withdrawal precautions

Question · Answer and explanation

Objective: glom-01, aki-11

The dipstick "blood" pad is a peroxidase reaction: it reacts with the iron-containing heme group and cannot tell whose heme it is — intact red cells, free hemoglobin from hemolysis, or myoglobin, the small oxygen-carrying protein of muscle, which filters freely and precipitates in acid urine into the pigmented granular casts you see. Heme-positive dipstick + no red cells on microscopy = hemoglobin or myoglobin (the dipstick–microscopy dissociation), and the 300 squats, the swollen thighs and a CK of 48,000 — far past the diagnostic threshold of five times the upper limit, about 1,000 U/L — name the pigment. CK is the stable detection marker; myoglobin, the injury agent, clears in hours, so no urine myoglobin level is needed.

Source-supported decision rule; faculty review pending.

• AAST rhabdomyolysis clinical consensus2022 — Management: optimal crystalloid/rate/urine-output goals; electrolyte abnormalities; complications

Question · Answer and explanation

Objective: lytes-17, aki-24

Pair the potassium with the ECG every time: 6.2 with peaked T waves means the heart is already affected, so calcium gluconate 1 g (10 mL of 10 %) IV goes first to stabilize the cardiac membrane — it removes no potassium and buys 30–60 minutes — while insulin with dextrose and albuterol shift potassium into cells and restored urine flow (Q8) removes it. Rhabdomyolysis lowers calcium because calcium binds injured muscle and precipitates with the phosphate flooding out of cells; that low calcium is otherwise left alone unless symptomatic (tetany, seizure, QT prolongation), because replacing it feeds the calcification and sets up rebound hypercalcemia in recovery. Tonight the calcium is given for the ECG, not for the number.

Source-supported decision rule; faculty review pending.

• AAST rhabdomyolysis clinical consensus2022 — Management: optimal crystalloid/rate/urine-output goals; electrolyte abnormalities; complications
• UKKA hyperkalemia guideline July 2026 — 14.1–14.2, 15.2–15.3, 16.2a–b

Question · Answer and explanation

Objective: aki-11, aki-23

Rhabdomyolysis injures the kidney three ways — myoglobin is toxic to tubular cells, it forms obstructing casts in acid urine, and the swollen muscle soaks up liters of fluid so the kidney is under-perfused as well — and goal-directed isotonic crystalloid answers all three by restoring perfusion and diluting the myoglobin. The AAST critical-care consensus summarized in the rhabdomyolysis handout starts at about 400 mL/h, titrated to a urine output of about 1–3 mL/kg/h (about 70–200 mL/h for her); the EAST 2022 guideline finds no support for routine bicarbonate or mannitol. The key word is titrated: reassess perfusion, lungs, balance and output every few hours, and if urine stops despite resuscitation, reassess for established AKI or overload rather than pouring in more.

Source-supported decision rule; faculty review pending.

• AAST rhabdomyolysis clinical consensus2022 — Management: optimal crystalloid/rate/urine-output goals; electrolyte abnormalities; complications

Question · Answer and explanation

Objective: aki-05, aki-04

FENa 0.6% supports sodium avidity and may increase the likelihood of a perfusion-related component in this clinical context. Diuretics affect the test, and low values can also occur with tubular injury, GN and other low-effective-volume states; this result neither proves fluid responsiveness nor excludes ATN. Use the history, examination, sediment and a carefully reassessed response to appropriate volume treatment. More likely is the preferred formative direction, with justified adjacent responses discussed rather than penalized.

Clinical application or calculation based on the cited principles; faculty review pending.

• Diagnostic performance of fractional excretion of urea and sodium in AKI2007 — Abstract: Methods, Results and Conclusions

Question · Answer and explanation

Objective: aki-08

Prerenal is a window, not a diagnosis you get to keep: hours at a mean pressure near 60 starved the proximal tubular cells, which do the most work on the least oxygen. Dead tubules cannot concentrate (specific gravity 1.010, the same as plasma) or hold sodium (FENa above 2 % — readable now, two days off the diuretic), and they wash out as muddy brown granular casts: ischemic ATN, now in its maintenance phase, which no drug shortens. With visible neck veins and 2.5 kg gained, more fluid can only find his lungs — fluid now matches losses, loop diuretics change the urine number but not the outcome and are kept for true overload, and low-dose dopamine is recommended against. Drugs are dosed to the trend (Q11), and nephrology is called: stage 3, not improving at 48–72 hours.

Clinical application or calculation based on the cited principles; faculty review pending.

• Diagnostic performance of fractional excretion of urea and sodium in AKI2007 — Abstract: Methods, Results and Conclusions
• Diagnostic value of urine microscopy for differential diagnosis of AKI2008 — Introduction; Methods; diagnostic sediment results

Question · Answer and explanation

Objective: aki-02, aki-25

Every creatinine-based estimate — CKD-EPI and Cockcroft–Gault alike — assumes steady state, so while creatinine is rising it overstates the filtration he has (the Part 1 pearl): dose for a clearance lower than the screen shows and re-dose as the trend turns, naming the estimate you used, using the kidney-function measure specified by the drug label. Metformin stays held until the creatinine is stable and the eGFR is at least 30. Gabapentin is almost entirely renally cleared, and 1,800 mg a day at a clearance in the teens means sedation, myoclonus and falls, so it drops to the bottom of its renal range rather than stopping cold. Enoxaparin accumulates below a clearance of 30 mL/min, so prophylaxis drops to the label dose for that range, with the recheck written into the order.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO CKD guideline 2024 — 1.3 GFR evaluation, pS175–S180; errors with non-steady state
• Gabapentin US prescribing information — 2.3 Table1 renal dosing; withdrawal precautions
• Lovenox US prescribing information — 2.3 Table1

Question · Answer and explanation

Objective: aki-22

Dialysis treats complications, not a creatinine, and the AEIOU list is the trigger to call now: Acidosis that will not correct (pH below about 7.1–7.2), Electrolytes (hyperkalemia still dangerous after calcium, insulin and a binder, or an ECG change that does not resolve), a dialyzable Intoxication (methanol, ethylene glycol, lithium, salicylates, metformin), volume Overload with pulmonary edema that a diuretic cannot clear, and Uremic pericarditis, encephalopathy or bleeding. Walter has none of them — potassium 5.8 with a quiet ECG, bicarbonate 17, clear lungs, eating breakfast — and dialysis started before a trigger appears does not improve survival. He needs what is already done — the nephrology call — and a team that re-examines him for the five triggers every shift, because ATN in its maintenance phase can still produce any of them.

Source-supported decision rule; faculty review pending.

• KDIGO AKI guideline 2012 — 5.1.1–5.1.2

Question · Answer and explanation

Objective: structural-01, structural-14

Non-contrast CT is highly accurate for an adult with suspected ureteral colic: it shows stone size and position, obstruction and alternative diagnoses. Ultrasound may precede CT and is preferred initially when radiation matters most, including pregnancy and children. Anuria, fever or a solitary kidney makes imaging urgent.

Source-supported decision rule; faculty review pending.

• EAU Urolithiasis guideline — 3.3 Diagnostic evaluation; imaging

Question · Answer and explanation

Objective: lytes-12

A potassium of 7.0 with PR prolongation and a widened QRS is a cardiac emergency. IV calcium stabilizes the myocardium without lowering potassium; reassess the ECG and repeat per the local resuscitation protocol if toxic changes persist. ECG changes do not progress in a reliable sequence, and a normal ECG would not make severe hyperkalemia safe.

Source-supported decision rule; faculty review pending.

• UKKA adult hyperkalemia guideline, July 2026 update — Guidelines 16–17; 17.1.2 potassium monitoring; 17.2 glucose monitoring, PDF pp14 and 113–114

Question · Answer and explanation

Objective: aki-07, aki-17, structural-06

Anuria (under 100 mL of urine a day) plus a rising creatinine in an older man with BPH is lower-tract obstruction until proven otherwise, and the fastest test is a bedside bladder scan (interpret the volume with the inability to void and the clinical setting). A bladder holding several hundred milliliters is acute retention: the Foley is both diagnosis and treatment, followed by a repeat BMP, a watch for post-obstructive diuresis, and an α-blocker (tamsulosin 0.4 mg daily) with urology follow-up. A blocked bladder outlet backs urine up into both kidneys at once, which is why it raises the creatinine.

Clinical application or calculation based on the cited principles; faculty review pending.

• NICE NG148 acute kidney injury — 1.3 recognition; 1.4.5–1.4.6 ultrasound; 1.5.1–1.5.3 obstruction and treatment

Question · Answer and explanation

Objective: aki-03, aki-07, aki-17, structural-14

A bladder scan answers one question — is urine pooling in the bladder? — and 0 mL says no; it says nothing about the ureter above. In a man with one kidney, one ureter, flank colic and no urine, an empty bladder is exactly what complete obstruction above the bladder looks like: nothing is getting past the stone. Renal ultrasound shows hydronephrosis (a dilated collecting system) at the bedside in minutes, with no radiation or contrast, and urology needs to hear about an obstructed solitary kidney now, while the potassium is treated in parallel.

Clinical application or calculation based on the cited principles; faculty review pending.

• NICE NG148 acute kidney injury — 1.3 recognition; 1.4.5–1.4.6 ultrasound; 1.5.1–1.5.3 obstruction and treatment
• EAU Urolithiasis guideline — 3.3 Diagnostic evaluation; imaging

Question · Answer and explanation

Objective: lytes-12, lytes-13, aki-22

Three jobs run in parallel: stabilize, shift, remove. Calcium protects the heart for 30–60 minutes, and insulin with dextrose plus high-dose albuterol pushes potassium into cells for a few hours, but none of them removes any. A loop diuretic needs urine flow he does not have; a binder does remove potassium through the gut whatever the urine output, but over hours — too slowly to be the emergency step. Removal here means relieving the obstruction, or dialysis if decompression is delayed or the potassium rebounds, so urology and nephrology are called now, not after the CT.

Source-supported decision rule; faculty review pending.

• UKKA adult hyperkalemia guideline, July 2026 update — Guidelines 16–17; 17.1.2 potassium monitoring; 17.2 glucose monitoring, PDF pp14 and 113–114
• EAU Urolithiasis guideline — 3.4.2 Management of sepsis and/or anuria in an obstructed kidney; 3.4.9 indications for ureteral-stone removal

Question · Answer and explanation

Objective: aki-03, aki-17, structural-07

Creatinine reflects total filtration. With two functioning kidneys, the unobstructed kidney often preserves enough filtration that an isolated ureteral stone causes little creatinine change. That protection is absent when the only functioning kidney is obstructed: total filtration falls and potassium and acid accumulate. Unilateral obstruction can still accompany AKI when the other kidney is impaired or additional injury is present.

Clinical application or calculation based on the cited principles; faculty review pending.

• EAU Urolithiasis guideline — 3.4.2 Management of sepsis and/or anuria in an obstructed kidney; 3.4.9 indications for ureteral-stone removal
• NICE NG148 acute kidney injury — 1.3 recognition; 1.4.5–1.4.6 ultrasound; 1.5.1–1.5.3 obstruction and treatment

Question · Answer and explanation

Objective: structural-02

NSAIDs are first-line for colic when both kidneys are healthy, but they block the prostaglandins that hold the afferent arteriole — the vessel feeding the glomerulus — open, and an underperfused, injured kidney may depend on that support. With stage 3 AKI, a potassium of 6.1 and three doses of ibuprofen already given, no NSAID dose is safe. An IV opioid titrated to effect, with acetaminophen as an adjunct, controls the pain without touching kidney perfusion, and a scheduled antiemetic keeps his oral medicines down.

Clinical application or calculation based on the cited principles; faculty review pending.

• Lapi et al. concurrent diuretic, ACEI/ARB and NSAID use and AKI — Abstract methods and results

Question · Answer and explanation

Objective: structural-05, structural-07

Two circumstances decide what this finding means: the kidney is obstructed, and the 37.9 °C triage reading was oral, in a man breathing 22 times a minute, five and a half hours after ibuprofen — an antipyretic. A stone alone can put white cells in the urine, but not bacteria, a positive nitrite and rigors; fever with that urine behind a blockage is infected obstruction, and a lactate of 3.1 with a falling blood pressure is sepsis physiology. Superimposed infection is now strongly supported. Anuria in the only kidney already required urgent drainage; these findings add sepsis resuscitation and antibiotics, not the first reason to act urgently.

Clinical application or calculation based on the cited principles; faculty review pending.

• EAU Urolithiasis guideline — 3.4.2 Management of sepsis and/or anuria in an obstructed kidney; 3.4.9 indications for ureteral-stone removal

Question · Answer and explanation

Objective: structural-02, structural-05, structural-07, aki-17

Infection behind an obstructed collecting system requires urgent drainage together with antibiotics and sepsis care. A stent or nephrostomy can provide source control; choose the feasible prompt route with the procedural team. Obtain cultures without materially delaying antibiotics. Use an appropriate initial antibiotic dose, then pharmacy-guided maintenance adjusted to the evolving kidney function, organism and infusion protocol; brisk urine output alone does not establish drug clearance.

Source-supported decision rule; faculty review pending.

• EAU Urolithiasis guideline — 3.4.2 Management of sepsis and/or anuria in an obstructed kidney; 3.4.9 indications for ureteral-stone removal
• NICE NG148 acute kidney injury — 1.3 recognition; 1.4.5–1.4.6 ultrasound; 1.5.1–1.5.3 obstruction and treatment
• Piperacillin-tazobactam prescribing information — Renal impairment dosage Table 1
• Ciprofloxacin prescribing information — 2.3 dosage modifications in renal impairment, Table 4

Question · Answer and explanation

Objective: aki-18, structural-08

Sustained urine output above 200 mL/h after decompression raises concern for post-obstructive diuresis. Follow intake, output, weight, blood pressure and electrolytes. Allow oral intake when safe and replace a tailored portion of losses intravenously if needed; select fluid composition from volume status and the sodium trend. Avoid automatically matching every milliliter, but do not permit hypovolemia. Sodium, potassium, magnesium and phosphorus need frequent checks, initially every 6–12 hours or more often if unstable.

Clinical application or calculation based on the cited principles; faculty review pending.

• NICE CG174 intravenous fluid therapy in adults — 1.1 assessment and monitoring; 1.3 resuscitation; 1.4 routine maintenance; 1.5 replacement and redistribution

Question · Answer and explanation

Objective: structural-03

Calcium oxalate points to low urine volume (his coffee-and-one-glass-of-water workday in a hot shop), high sodium, excess animal protein and sometimes low citrate or high oxalate, so every former gets fluids, less sodium, moderate protein and normal calcium (1,000–1,200 mg/day with meals). The 24-hour urine is for recurrent formers and high-risk first-time formers, and a man whose next stone could again block his only kidney is high-risk. Collect twice on his usual diet, several weeks after the episode and the procedure, and let the results choose the drug: a thiazide for hypercalciuria, potassium citrate for hypocitraturia.

Source-supported decision rule; faculty review pending.

• EAU metabolic evaluation and recurrence prevention — 4.1.2 urine sampling; 4.2 general preventive measures

Question · Answer and explanation

Objective: lytes-15

About half of blood calcium rides on albumin, so a low albumin makes the total read low while the free (ionized) calcium — the part that acts on nerves, muscle and kidney — is unchanged. Add 0.8 mg/dL for every 1 g/dL of albumin below 4.0: 11.2 + 0.8 × (4.0 − 2.4) = 11.2 + 1.28 = 12.5 mg/dL, giving an estimated corrected value of 12.5. Albumin-correction formulas can misclassify calcium status; confirm with ionized calcium when the result will change management, especially during critical illness or marked hypoalbuminemia.

Clinical application or calculation based on the cited principles; faculty review pending.

• Society for Endocrinology emergency management of acute hypercalcemia — Investigations and management sections

Question · Answer and explanation

Objective: lytes-15

When calcium is high, healthy parathyroid glands switch off and PTH falls below about 15–20 pg/mL, so the PTH result splits the differential in two. PTH high or "inappropriately normal" means the glands are driving it (primary hyperparathyroidism, lithium, rarely familial hypocalciuric hypercalcemia); PTH suppressed means something else is raising the calcium and the glands are correctly silent (malignancy, vitamin D excess, granulomatous disease, milk-alkali, immobilization). Every other test on this list is chosen by the branch.

Source-supported decision rule; faculty review pending.

• Society for Endocrinology emergency management of acute hypercalcemia — Investigations and management sections

Question · Answer and explanation

Objective: structural-23

At a steady-state eGFR of 27, stop metformin and revise the diabetes plan: the FDA label contraindicates it below 30 mL/min/1.73 m². The label discourages initiation at 30–45 and calls for a benefit–risk review when an established user falls below 45. Hold during AKI or a dehydrating acute illness. Contrast policies differ: the ACR–NKF approach requires withholding in AKI or eGFR below 30; the FDA label is stricter, also requiring withholding for iodinated contrast at eGFR 30–60 and in specified additional risk settings, then reassessment after 48 hours. State which policy the service uses. Neither policy changes this answer at eGFR 27.

Source-supported decision rule; faculty review pending.

• Metformin prescribing information — 2.3 renal impairment; 2.4 iodinated contrast
• ACR–NKF consensus on intravenous iodinated contrast — Consensus statements on high-risk patients, prophylaxis and metformin

Question · Answer and explanation

Objective: aki-27, lytes-16

Creatinine-bump triage turns on symptoms, potassium, urine output and trajectory, and here the symptoms decide it: a creatinine more than double its baseline with a corrected calcium above 14 and new confusion is a same-day emergency, not a recheck. Calcium at this level dulls the gut and the brain, shortens the QT interval, and drains the kidney of water and blood flow. He needs IV isotonic saline on a cardiac monitor today, and the workup travels with him.

Source-supported decision rule; faculty review pending.

• Society for Endocrinology emergency management of acute hypercalcemia — Investigations and management sections
• Endocrine Society hypercalcemia of malignancy guideline — Recommendations 1–3

Question · Answer and explanation

Objective: aki-03, aki-04

Volume depletion and calcium-associated renal vasoconstriction are the leading contributors here. Hypercalcemia can impair urinary concentration, causing water loss; the orthostasis and weight loss support depleted volume. Ultrasound shows no obstruction and the urine lacks inflammatory clues, but neither a bland sediment nor a normal ultrasound completely excludes intrinsic injury or early obstruction. Follow recovery with treatment and reassess if it is incomplete.

Clinical application or calculation based on the cited principles; faculty review pending.

• Society for Endocrinology emergency management of acute hypercalcemia — Investigations and management sections
• NICE NG148 acute kidney injury — 1.3 recognition; 1.4.5–1.4.6 ultrasound; 1.5.1–1.5.3 obstruction and treatment

Question · Answer and explanation

Objective: lytes-15

A PTH of 8 puts him on the PTH-independent branch, and at a calcium of 14.4 that branch's tests go out together: PTHrP (a tumor-made look-alike of PTH — kidney, squamous lung and head-and-neck cancers), 25-OH vitamin D (supplement excess) and 1,25-(OH)₂ vitamin D (granulomas, lymphoma), SPEP with serum free light chains and a UPEP (myeloma), and a chest film for a smoker's lung cancer or hilar nodes. Three causes need a history, not a lab: milk-alkali (calcium carbonate + metabolic alkalosis + AKI — he has all three), the thiazide, and immobilization (he walks).

Clinical application or calculation based on the cited principles; faculty review pending.

• Society for Endocrinology emergency management of acute hypercalcemia — Investigations and management sections

Question · Answer and explanation

Objective: lytes-16

Severe symptomatic hypercalcemia needs rehydration plus prompt calcium-lowering therapy. Calcitonin provides an early bridge and should be limited to 48–72 hours because its effect wanes. For suspected malignancy-associated hypercalcemia, an IV bisphosphonate or denosumab supplies the sustained effect; choose promptly with the specialist, considering renal function, infusion/dose guidance and hypocalcemia risk. Do not wait indefinitely for creatinine to normalize. A loop diuretic is reserved for volume overload.

Source-supported decision rule; faculty review pending.

• Endocrine Society hypercalcemia of malignancy guideline — Recommendations 1–3
• Society for Endocrinology emergency management of acute hypercalcemia — Investigations and management sections

Question · Answer and explanation

Objective: glom-06

Red cells that cross a damaged glomerulus arrive misshapen (dysmorphic, acanthocytes, sometimes packed into casts) and usually travel with protein; isomorphic cells favor a nonglomerular source but do not prove it. Isomorphic cells with no protein or casts, visible bleeding, a man in his sixties and 48 pack-years put him in the AUA/SUFU high-risk group: upper-tract imaging and cystoscopy, not a repeat dipstick. Tumors bleed intermittently, so hematuria that stops has not been explained — and the later mass reinforces why the earlier bleeding needed investigation.

Source-supported decision rule; faculty review pending.

• AUA/SUFU 2025 microhematuria diagnostic algorithm — Definition, risk stratification and evaluation algorithm

Question · Answer and explanation

Objective: lytes-15

The circumstance to notice is that milk-alkali suppresses PTH too, so the PTH of 8 only chose the branch — it could not separate the benign story (he has the whole milk-alkali triad) from the malignant one. PTHrP can: antacids and thiazides cannot make it, tumors do, and the same tumor explains the weight loss, the hematuria and the vascular mass. At 3.4 times the upper limit, milk-alkali falls to much less likely as the main cause — though the carbonate and the thiazide still added calcium and built the alkalosis, so they stay stopped.

Clinical application or calculation based on the cited principles; faculty review pending.

• Society for Endocrinology emergency management of acute hypercalcemia — Investigations and management sections

Question · Answer and explanation

Objective: aki-10, structural-14, structural-15

Given the stated availability and diagnostic adequacy, contrast MRI with a group II agent answers the question while avoiding iodinated contrast. ACR–NKF considers the NSF risk from group II agents very low even in advanced kidney dysfunction; very low is not zero. Needed iodinated contrast is also permissible after a risk–benefit assessment in AKI, with appropriate prophylaxis when indicated. It is a relative risk, not a blanket prohibition.

Source-supported decision rule; faculty review pending.

• ACR–NKF consensus on intravenous iodinated contrast — Consensus statements on high-risk patients, prophylaxis and metformin
• ACR–NKF consensus on gadolinium-based contrast — Summary and group II GBCA risk statements

Question · Answer and explanation

Objective: structural-12, aki-26

The imaging describes a Bosniak I simple cyst, so it needs no routine surveillance unless symptomatic. The AKI needs its own follow-up: document the episode, arrange an early creatinine and medication review within about 1–2 weeks after discharge (sooner if unstable), then assess renal recovery, blood pressure, urinalysis and UACR by 3 months. Drug restart and dosing follow clinical recovery and stable renal estimates, not the cyst classification.

Clinical application or calculation based on the cited principles; faculty review pending.

• CUA 2023 cystic renal lesion guideline — Recommendations 4–6 and Bosniak management section
• NICE NG148 acute kidney injury — 1.3 recognition; 1.4.5–1.4.6 ultrasound; 1.5.1–1.5.3 obstruction and treatment

Question · Answer and explanation

Objective: structural-13

Enhancement plus hematuria and systemic symptoms warrants evaluation for malignancy. Incidental detection and absent classic signs do not establish benignity. CT/MRI cannot reliably distinguish every RCC from oncocytoma or fat-poor angiomyolipoma. Urology selects further evaluation and management; biopsy is useful selectively, not mandatory before referral or every operation. The EAU RCC guideline, sections 5.1–5.3, supports these distinctions.

Source-supported decision rule; faculty review pending.

• EAU renal cell carcinoma guideline — 5.1 symptoms; 5.2 imaging including CT/MRI limitations; 5.3.1 biopsy indications

Question · Answer and explanation

Objective: aki-13, ckd-19, structural-20

Prostaglandins hold the afferent arteriole — the small artery feeding each filter (glomerulus) — open. Her diuretic shrinks her volume and her ACE inhibitor removes the efferent squeeze that props up filtration pressure, so that dilation is the last support left; take it away and filtration falls within a day or two, with a bland urine, and recovers when the drug stops. Diuretic + RAAS blocker + NSAID is the "triple whammy" , and its risk is highest in the first 30 days.

Clinical application or calculation based on the cited principles; faculty review pending.

• Lapi et al. concurrent diuretic, ACEI/ARB and NSAID use and AKI — Abstract methods and results

Question · Answer and explanation

Objective: aki-14

A small early creatinine rise can follow reduced intraglomerular pressure with ACE inhibition. In this well patient, 1.0 to 1.2 is 20%, so continue and recheck creatinine and potassium. KDIGO 2024 advises reassessment when creatinine rises more than 30% within 4 weeks: look for volume depletion, interacting drugs and renovascular disease, and reduce or stop if the problem cannot be corrected. Symptomatic hypotension or uncontrolled hyperkalemia can also require adjustment. A rise is not required to prove benefit.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — Practice Points 3.6.2, 3.6.4, 3.6.5

Question · Answer and explanation

Objective: ckd-18

Colchicine is cleared by CYP3A4 — a drug-metabolizing enzyme in the liver and the gut wall — and pumped out of cells by P-glycoprotein, and clarithromycin blocks both. On an unchanged dose the level climbs, and colchicine has a narrow window: diarrhea, muscle injury and a falling blood count are its toxicity, worse when kidney function is reduced. This combination is contraindicated in renal impairment: stop the interacting drugs and arrange urgent toxicity assessment. The rule travels: when a narrow-window drug is cleared by CYP3A4, a new inhibitor raises its level and a new inducer lowers it.

Source-supported decision rule; faculty review pending.

• Colchicine prescribing information — 4 contraindications; 5.2–5.4 blood dyscrasias, interactions and neuromuscular toxicity

Question · Answer and explanation

Objective: aki-27, structural-27

Three things take her out of the 48–72-hour lane: a potassium of 5.8 that needs an ECG today; a creatinine 1.67 times her baseline — the size of a KDIGO stage 1 rise, although with the last value four weeks old the 7-day clock cannot be applied ; and new symptoms in a patient whose only working kidney is a transplant. The outpatient creatinine-bump work-up is the usual one — confirm the change, review the medications, check the urine and the bladder, assess volume — and in a transplant recipient it adds a tacrolimus level and a same-day call to the center.

Clinical application or calculation based on the cited principles; faculty review pending.

• Tacrolimus prescribing information — Warnings: nephrotoxicity, neurotoxicity, hyperkalemia and hypertension; CYP3A drug interactions
• UKKA adult hyperkalemia guideline, July 2026 update — Guidelines 16–17; 17.1.2 potassium monitoring; 17.2 glucose monitoring, PDF pp14 and 113–114

Question · Answer and explanation

Objective: structural-27

Ibuprofen on top of lost volume explains a creatinine rise (W1's afferent squeeze) and can raise the potassium, because NSAIDs lower renin and with it aldosterone. That explanation does not adequately account for the new tremor and worsening glucose on an unchanged prednisone dose; stress can raise glucose, so these are supporting clues rather than proof; the headaches could belong to either story. Two findings outside the first story mean a second process — in a tacrolimus patient, what a level above range looks like, which is why a level was added to this morning's sample. Whether it is high, and whether it also explains the creatinine, the result will say.

Clinical application or calculation based on the cited principles; faculty review pending.

• Tacrolimus prescribing information — Warnings: nephrotoxicity, neurotoxicity, hyperkalemia and hypertension; CYP3A drug interactions

Question · Answer and explanation

Objective: structural-27

When a stable patient destabilizes on an unchanged dose, look for the new drug that changed how the old one is cleared — read the medication list by start date. Tacrolimus is broken down by CYP3A4 in the liver and gut wall and pumped back out of gut cells by P-glycoprotein; diltiazem and verapamil, the heart-rate-slowing (non-dihydropyridine) calcium-channel blockers, block both, so the same 3 mg gives a higher level. Azole antifungals, clarithromycin and erythromycin, and grapefruit juice do the same; the inducers rifampin, phenytoin, carbamazepine and St John's wort push the level down and risk rejection.

Source-supported decision rule; faculty review pending.

• Tacrolimus prescribing information — Warnings: nephrotoxicity, neurotoxicity, hyperkalemia and hypertension; CYP3A drug interactions

Question · Answer and explanation

Objective: lytes-14

Compute the gap before you name the acidosis: 137 − (107 + 19) = 11, inside this lab's 8–12, and an albumin of 4.0 needs no correction. A normal-gap acidosis with high potassium points to the collecting duct: aldosterone normally drives sodium in and potassium and acid out, and when the duct cannot respond — type 4 renal tubular acidosis (RTA) — both are retained, giving a mild acidosis (bicarbonate 17–24) with potassium 5.5–7.0 and a urine that can still acidify. High tacrolimus does this, NSAIDs add to it, and correcting the contributors may improve the bicarbonate. This is a type 4 pattern, not a definitive isolated RTA diagnosis from one BMP; the center directs any tacrolimus change.

Clinical application or calculation based on the cited principles; faculty review pending.

• Tacrolimus prescribing information — Warnings: nephrotoxicity, neurotoxicity, hyperkalemia and hypertension; CYP3A drug interactions

Question · Answer and explanation

Objective: aki-27, ckd-19, structural-27

Remove ibuprofen, assess and correct volume loss, review potassium intake and repeat potassium promptly. A normal ECG does not exclude dangerous hyperkalemia. Discuss disposition with the transplant center now; outpatient follow-up is acceptable only if repeat results and the clinical assessment support it and rapid re-evaluation is reliable. Escalate to the ED if potassium rises, symptoms develop or timely reassessment is unavailable. The center directs any immunosuppression change.

Clinical application or calculation based on the cited principles; faculty review pending.

• Tacrolimus prescribing information — Warnings: nephrotoxicity, neurotoxicity, hyperkalemia and hypertension; CYP3A drug interactions
• UKKA adult hyperkalemia guideline, July 2026 update — Guidelines 16–17; 17.1.2 potassium monitoring; 17.2 glucose monitoring, PDF pp14 and 113–114

Question · Answer and explanation

Objective: structural-27, aki-03

Notice the clock first: she takes tacrolimus at 8 a.m. and 8 p.m., so a 07:45 draw is a true trough — the same 18 drawn an hour after a dose would mean little. A true trough more than double her target, on a dose unchanged for fourteen months and four weeks after a CYP3A4 inhibitor started, explains the whole board (creatinine, tremor, potassium and acid, magnesium, glucose), where the ibuprofen-and-diarrhea story explains only the creatinine and the potassium. The two stories do not compete: persistent diarrhea can raise tacrolimus exposure, so it fed the same problem — the NSAID is demoted, not discarded, and it still had to go.

Clinical application or calculation based on the cited principles; faculty review pending.

• Tacrolimus prescribing information — Warnings: nephrotoxicity, neurotoxicity, hyperkalemia and hypertension; CYP3A drug interactions

Question · Answer and explanation

Objective: structural-27

Implement the center's plan: stop diltiazem, communicate the exact time and have the center adjust tacrolimus and schedule troughs. Exposure can change over the ensuing days, with variable timing. Continued creatinine elevation despite correction of exposure and volume requires reassessment for other allograft problems.

Source-supported decision rule; faculty review pending.

• Tacrolimus prescribing information — Warnings: nephrotoxicity, neurotoxicity, hyperkalemia and hypertension; CYP3A drug interactions

Question · Answer and explanation

Objective: htn-cardiorenal-07, htn-cardiorenal-08

Match the agent to the patient: ACE inhibitors and ARBs raise potassium, and diltiazem and verapamil raise tacrolimus. Amlodipine, a dihydropyridine calcium-channel blocker (a different subclass from diltiazem), does not usually raise potassium and needs no renal dose adjustment, but can increase tacrolimus exposure; the center checks a trough after it starts, and ankle edema is the side effect to warn about. Her target is below 130/80 (2025 AHA/ACC); KDIGO's lower systolic target of 120 explicitly excludes transplant recipients .

Clinical application or calculation based on the cited principles; faculty review pending.

• Tacrolimus prescribing information — Warnings: nephrotoxicity, neurotoxicity, hyperkalemia and hypertension; CYP3A drug interactions
• KDIGO 2024 CKD guideline — Practice Points 3.6.2, 3.6.4, 3.6.5

Question · Answer and explanation

Objective: structural-27, ckd-20

Three checklist items in one call. Patients should not independently interrupt immunosuppression: missed doses risk rejection and illness can alter exposure. The transplant center may intentionally hold or adjust a drug and directs the dose, route and monitoring. Clarithromycin is a CYP3A4 inhibitor that would do to her trough in days what diltiazem did in weeks; the nasal-spray influenza vaccine is live (she gets the injected inactivated one); and a fever in an immunosuppressed patient is a same-day call.

Clinical application or calculation based on the cited principles; faculty review pending.

• Tacrolimus prescribing information — Warnings: nephrotoxicity, neurotoxicity, hyperkalemia and hypertension; CYP3A drug interactions
• Colchicine prescribing information — 4 contraindications; 5.2–5.4 blood dyscrasias, interactions and neuromuscular toxicity

Question · Answer and explanation

Objective: htn-cardiorenal-13

Spells of headache, palpitations and sweating, with pressure high during the spell and normal between, is the pheochromocytoma pattern — a catecholamine-secreting tumor of the adrenal medulla. The screen is biochemical: plasma free metanephrines (breakdown products of epinephrine and norepinephrine, and the most sensitive test) or a 24-hour urine for fractionated metanephrines; imaging comes only after a positive result. He is referred before any procedure because alpha-blockade must be in place before a beta-blocker or an operation.

Source-supported decision rule; faculty review pending.

• Endocrine Society pheochromocytoma/paraganglioma guideline — Initial biochemical testing recommendation; PubMed abstract PMID24893135

Question · Answer and explanation

Objective: htn-cardiorenal-01, htn-cardiorenal-02

Repeat after at least 5 minutes of seated rest with the back, feet and arm supported and an appropriately sized cuff; average repeated readings without conversation. Confirm sustained hypertension with a validated home or ambulatory device. This case uses two readings each morning and evening, at least one minute apart, over 7 days, averaging days 2–7.

Clinical application or calculation based on the cited principles; faculty review pending.

• AHA/ACC 2025 high blood pressure guideline highlights — Items 4–10

Question · Answer and explanation

Objective: htn-cardiorenal-15

Retinal hemorrhages and a creatinine that has more than doubled in four months are acute target-organ damage, so this is a hypertensive emergency: a titratable IV drug (nicardipine or labetalol) in a monitored bed. His mean arterial pressure (MAP), (224 + 2 × 128) ÷ 3 = 160, comes down by no more than about 25% in the first hour (to about 120), then toward 160/100 over 2–6 hours, because autoregulation has reset upward and a faster fall causes ischemia. Two conditions carry their own targets: aortic dissection (systolic under 120 within 20 minutes) and severe preeclampsia (140–150/90–100 within 30–60 minutes).

Clinical application or calculation based on the cited principles; faculty review pending.

• AHA/ACC 2025 high blood pressure guideline highlights — Items 4–10

Question · Answer and explanation

Objective: htn-cardiorenal-02, htn-cardiorenal-03

Office ≥140 systolic or ≥90 diastolic is stage 2, and a home average of 130/80 or higher makes it sustained, not white-coat. Stage 2 is drug-first whatever the PREVENT score (the AHA 10-year cardiovascular risk calculator, whose 7.5% threshold decides stage 1 only). The second half is the point of the case: onset before 30, in a young woman on an estrogen pill, with an epigastric bruit, is a cluster of secondary-hypertension red flags — so you treat and investigate in parallel.

Source-supported decision rule; faculty review pending.

• AHA/ACC 2025 high blood pressure guideline highlights — Items 4–10

Question · Answer and explanation

Objective: htn-cardiorenal-06, htn-cardiorenal-11, htn-cardiorenal-14

Stop the estrogen-containing pill and offer reliable alternative contraception. Treat the confirmed hypertension while arranging aldosterone/renin testing. Drugs can change renin, aldosterone or both; the direction and magnitude matter. Amlodipine is a reasonable interim choice but may lower the ratio, so the screen is not entirely free of confounding. Do not withhold needed BP treatment merely to obtain an ideal test; use the 2025 guideline's feasible medication strategy and repeat testing when appropriate.

Clinical application or calculation based on the cited principles; faculty review pending.

• AHA/ACC 2025 high blood pressure guideline highlights — Items 4–10
• Endocrine Society 2025 primary aldosteronism guideline — Recommendations 1 and 3; technical remarks

Question · Answer and explanation

Objective: lytes-11, lytes-25

Low potassium and elevated bicarbonate indicate hypokalemic metabolic alkalosis. A urine chloride of 48 makes remote vomiting or a remote diuretic effect less likely, but does not by itself prove normal volume or mineralocorticoid excess. The hypertension distinguishes this pattern from typical salt-wasting tubulopathies. The urine potassium concentration supports ongoing urinary loss in context; a spot concentration alone is not a quantitative potassium-excretion rate.

Clinical application or calculation based on the cited principles; faculty review pending.

• Endocrine Society 2025 primary aldosteronism guideline — Recommendations 1 and 3; technical remarks

Question · Answer and explanation

Objective: htn-cardiorenal-11

Screen with morning seated aldosterone and renin after correcting potassium, using the laboratory's assay and units. A positive screen requires the combined pattern of suppressed renin, inappropriately high aldosterone and an elevated ratio; the ratio alone is insufficient. Review medication interference. Withdrawal of interfering drugs, including MRAs, is useful when safe, but no- or minimal-withdrawal strategies are possible. Amlodipine is a practical interim choice but can lower the ratio; repeat a negative result if suspicion remains high. Imaging follows biochemical evaluation.

Source-supported decision rule; faculty review pending.

• Endocrine Society 2025 primary aldosteronism guideline — Recommendations 1 and 3; technical remarks

Question · Answer and explanation

Objective: htn-cardiorenal-11, htn-cardiorenal-12

Primary aldosteronism usually suppresses renin. Here renin is high and the ratio low, which weakens that hypothesis and, with the bruit, supports a renovascular cause. The result is not an absolute exclusion: medication effects remain possible, including amlodipine. A negative screen with continuing high suspicion needs repeat testing under an appropriate medication strategy.

Clinical application or calculation based on the cited principles; faculty review pending.

• Endocrine Society 2025 primary aldosteronism guideline — Recommendations 1 and 3; technical remarks
• First international consensus on fibromuscular dysplasia — Renal angiography and revascularization, PDF16 / printed17

Question · Answer and explanation

Objective: htn-cardiorenal-12, structural-16, htn-cardiorenal-08

A beaded mid-to-distal artery, a clean aorta and equal kidneys in a young woman without vascular risk factors is fibromuscular dysplasia — the form of renal artery stenosis in which balloon angioplasty can improve or sometimes cure hypertension in selected patients; stenting is usually reserved for complications, so the referral belongs in the first plan. Renovascular hypertension is renin-driven, so an ACE inhibitor works well, and with unilateral disease the other kidney holds the GFR; the safety net is a BMP at 1–2 weeks, accepting a creatinine rise up to 30%. Amlodipine continues, and because ACE inhibitors harm a fetus, she needs reliable contraception.

Clinical application or calculation based on the cited principles; faculty review pending.

• First international consensus on fibromuscular dysplasia — Renal angiography and revascularization, PDF16 / printed17

Question · Answer and explanation

Objective: htn-cardiorenal-18, htn-cardiorenal-08, structural-17

ACE inhibitors and ARBs injure the fetal kidney — oligohydramnios (too little amniotic fluid, because the fetal kidneys stop making urine), renal dysgenesis and neonatal kidney failure — with the clearest harm later in pregnancy and possible first-trimester risk, so the drug stops the day pregnancy is known. Her hypertension was controlled on treatment, so she stays treated: the CHAP trial found that treating chronic hypertension in pregnancy to below 140/90 reduced serious complications without harming fetal growth. Labetalol (an alpha- and beta-blocker) and extended-release nifedipine are first-line; methyldopa is an older, less effective alternative.

Source-supported decision rule; faculty review pending.

• Treatment for mild chronic hypertension during pregnancy (CHAP) — Abstract methods and conclusion
• ACOG Committee Opinion 767: emergent therapy for acute severe hypertension — Abstract

Question · Answer and explanation

Objective: htn-cardiorenal-18, structural-17

Severe-range pressure (systolic ≥160 or diastolic ≥110) in pregnancy, confirmed over 15 minutes, is treated within 30–60 minutes — delay is what causes maternal stroke — with IV labetalol, IV hydralazine or oral immediate-release nifedipine (never sublingual). The target is 140–150/90–100, not normal, because overshooting under-perfuses the placenta. Magnesium sulfate prevents eclampsia (seizures) in preeclampsia with severe features, and delivery is the only cure: at 34 weeks the obstetric team delivers once the mother is stable, and the student's job is to recognize the cluster, treat on the clock and call.

Source-supported decision rule; faculty review pending.

• ACOG Practice Bulletin 222: gestational hypertension and preeclampsia, interim update — PDF8/e245 delivery ≥34 weeks; PDF10/e247 magnesium; PDF15/e252 severe hypertension summary
• ACOG Committee Opinion 767: emergent therapy for acute severe hypertension — Abstract

Question · Answer and explanation

Objective: htn-cardiorenal-18, htn-cardiorenal-15

Persistent systolic pressure at least 160 or diastolic pressure at least 110 in the postpartum period needs urgent treatment, with the same 30–60-minute window used in pregnancy. Recent HELLP and a new severe headache warrant obstetric assessment, repeat labs and magnesium for suspected postpartum preeclampsia with severe features. A normal head CT does not exclude every neurologic complication. In a nonpregnant patient, headache likewise requires assessment before concluding that target-organ injury is absent; it is not an automatic outpatient-discharge rule.

Source-supported decision rule; faculty review pending.

• ACOG Practice Bulletin 222: gestational hypertension and preeclampsia, interim update — PDF8/e245 delivery ≥34 weeks; PDF10/e247 magnesium; PDF15/e252 severe hypertension summary
• ACOG Committee Opinion 767: emergent therapy for acute severe hypertension — Abstract

Question · Answer and explanation

Objective: glom-06

The sediment sorts hematuria onto two roads. Red cells that crossed a damaged glomerulus come out misshapen (dysmorphic), often in casts and with protein: nephrology. Uniform cells without casts or substantial protein favor a nonglomerular source but do not prove it: urology, where the AUA/SUFU guideline sets how hard to look from age, sex, smoking and the amount of blood. Microhematuria is at least 3 RBC/hpf on microscopy, not a dipstick reading; she has 12.

Clinical application or calculation based on the cited principles; faculty review pending.

• AUA/SUFU 2025 microhematuria diagnostic algorithm — Definition, risk stratification and evaluation algorithm

Question · Answer and explanation

Objective: structural-01, structural-14

Non-contrast CT is the reference test for a suspected stone: highly accurate, it shows the uric-acid stones a plain film misses and gives size, position and the degree of obstruction (hydronephrosis — a kidney swollen because urine cannot drain), and it finds the other diagnosis when it is not a stone. A stone is visible without contrast, so none is given. Ultrasound comes first in pregnancy and in children; it shows hydronephrosis well but misses many ureteral stones.

Source-supported decision rule; faculty review pending.

• EAU Urolithiasis guideline — 3.3 Diagnostic evaluation; imaging

Question · Answer and explanation

Objective: structural-15

The 2020 ACR–NKF consensus treats the kidney risk of IV contrast as very low above an eGFR of 30, and names eGFR below 30, or AKI, as the group in whom isotonic fluid around the scan is reasonable. Even in that group a scan that changes management is done — a missed bowel infarction is far more dangerous than a creatinine bump.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2025 ADPKD guideline, corrected April 2026 PDF — 6.1 Recommendation 2; Practice Points 6.1.10–6.1.11

Question · Answer and explanation

Objective: ckd-08, structural-01, structural-14

In a polycystic kidney, flank pain with blood has three causes, sorted in two moves. Fever and systemic illness raise concern for infection; being afebrile lowers that concern but cannot alone exclude it. The non-contrast CT separates a stone from bleeding into a cyst: about one in five people with ADPKD forms stones, colicky waves are a stone until proven otherwise, and ultrasound misses many ureteral stones. The same scan shows whether a cyst is denser than water — the look of fresh blood.

Source-supported decision rule; faculty review pending.

• KDIGO 2025 ADPKD guideline, corrected April 2026 PDF — 1.3 diagnosis; Practice Point 1.3.5 and Figures 3–5, PDF23 and 65–66

Question · Answer and explanation

Objective: structural-10, structural-14, ckd-08

His first-degree family history of subarachnoid hemorrhage is an indication to discuss intracranial aneurysm screening, provided he would be eligible for treatment and has a reasonable life expectancy. Non-contrast time-of-flight MRA is the preferred screening study. A negative study may be repeated in 5–10 years according to individual risk and preferences. A thunderclap headache is an emergency requiring diagnostic evaluation, not a routine screening indication.

Source-supported decision rule; faculty review pending.

• KDIGO 2025 ADPKD guideline, corrected April 2026 PDF — 6.1 Recommendation 2; Practice Points 6.1.10–6.1.11

Question · Answer and explanation

Objective: ckd-10, htn-cardiorenal-07

Hypertension affects 50–70 % of people with ADPKD, often in their thirties and before kidney function falls, because growing cysts squeeze the kidney's blood supply and switch on renin. An ACE inhibitor (or ARB) is first-line: check creatinine and potassium at 1–2 weeks and accept a rise of up to 30 %. Aim below 130/80 (2025 AHA/ACC); the lower HALT-PKD and KDIGO targets are the nephrologist's call. The NSAID goes for good — it raises the pressure and threatens a kidney already under strain.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2024 CKD guideline — Practice Points 3.6.2, 3.6.4, 3.6.5
• KDIGO 2024 CKD guideline — 3.3.1 protein; 3.3.2 sodium; 3.10 acidosis

Question · Answer and explanation

Objective: structural-10, glom-06

Acute flank pain, gross hematuria and a stable hemoglobin is the classic picture of a cyst bleed, managed conservatively; the urine usually clears within days to a couple of weeks. The Session 3 rule rides along: blood is never attributed to a cause until it is shown to clear, so the 2–4-week urinalysis is part of the plan, and isomorphic hematuria that persists goes to urology. And no NSAIDs again — acetaminophen is his analgesic.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2025 ADPKD guideline, corrected April 2026 PDF — 1.3 diagnosis; Practice Point 1.3.5 and Figures 3–5, PDF23 and 65–66
• AUA/SUFU 2025 microhematuria diagnostic algorithm — Definition, risk stratification and evaluation algorithm

Question · Answer and explanation

Objective: structural-09

Screening an at-risk adult is a conversation before it is a scan, and at 19 the choice is his. He needs the facts first: a 50 % prior risk; a positive scan that brings lifelong blood-pressure care but also a diagnosis in his record, with consequences for life and disability insurance; and a negative scan that is reassuring but provisional, because cysts accumulate with age — it is repeated every few years, and the reassurance from a negative ultrasound depends on age, familial genotype and the purpose of testing; a negative study at 19 cannot definitively clear a potential future donor. Ultrasound is the right first test: cheap, no radiation, no contrast.

Source-supported decision rule; faculty review pending.

• KDIGO 2025 ADPKD guideline, corrected April 2026 PDF — 1.3 diagnosis; Practice Point 1.3.5 and Figures 3–5, PDF23 and 65–66

Question · Answer and explanation

Objective: structural-09, structural-12

She asked one question and is owed two answers. Is the cyst dangerous? No: a thin wall, no septa and nothing inside make a simple cyst — the ultrasound equivalent of Bosniak I — and it needs no follow-up (IIF lesions are re-imaged; III and IV go to urology). Does she have her father's disease? A different rule: at 15–39 the diagnosis needs three cysts, and fewer than two cysts at 40 or older can exclude typical familial PKD1/PKD2 disease under the established age-specific criteria, so at 38 with one cyst she is neither diagnosed nor cleared. A scan at 40 can clear her; genetic testing is faster if she cannot wait.

Source-supported decision rule; faculty review pending.

• KDIGO 2025 ADPKD guideline, corrected April 2026 PDF — 1.3 diagnosis; Practice Point 1.3.5 and Figures 3–5, PDF23 and 65–66
• CUA 2023 cystic renal lesion guideline — Recommendations 4–6 and Bosniak management section

Question · Answer and explanation

Objective: structural-05, structural-10

A man with fever, rigors and a structurally abnormal kidney has a complicated urinary infection, and this systemically unwell, rigoring patient needs hospital assessment and inpatient treatment. Order matters: blood and urine cultures before the first dose, then an IV agent — ceftriaxone is the usual inpatient start. Ask nephrology and infectious disease on day one which drug reaches cyst fluid (the lecture page names fluoroquinolones first, TMP-SMX second), and image again if he is not better at 48–72 hours. The lisinopril is held under the Session 2 sick-day rule.

Source-supported decision rule; faculty review pending.

• KDIGO 2025 ADPKD guideline, corrected April 2026 PDF — 2.6.5 kidney cyst infection, PDF96–97 / S95–S96

Question · Answer and explanation

Objective: structural-05, structural-10

Persistent fever despite initial treatment, sterile pre-antibiotic urine and the ADPKD context shift concern toward an infected cyst that may not communicate with the collecting system. A negative culture does not rule out pyelonephritis, and cyst infection and pyelonephritis can coexist. Reassess the whole patient and alternative sources, use appropriate imaging and discuss cyst-penetrating therapy with nephrology and infectious disease. This finding supports the hypothesis; it does not establish it.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2025 ADPKD guideline, corrected April 2026 PDF — 2.6.5 kidney cyst infection, PDF96–97 / S95–S96

Question · Answer and explanation

Objective: ckd-22, ckd-24

Transplant referral belongs in G4, no later than an eGFR of about 20, so evaluation and a living-donor work-up finish before dialysis is needed; a pre-emptive transplant from a living relative is the best kidney he can get. KRT education starts now (in-center and home hemodialysis, peritoneal dialysis, transplant, conservative care); dialysis, if it comes, starts for symptoms, not a number. Preserve suitable arm and central veins and discuss any PICC with the kidney team; access side is chosen through the individual vascular-access plan. Four negative scans at 34 do not exclude ADPKD, so the brother is confirmed unaffected, by genetic testing if needed.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — 5.4 Practice Points 1–3 and Table 41; 5.5 comprehensive conservative care
• KDIGO 2024 CKD guideline — Practice Points 2.2.1–2.2.3; Figure 48, printed S255 / PDF139
• KDIGO 2025 ADPKD guideline, corrected April 2026 PDF — 1.3 diagnosis; Practice Point 1.3.5 and Figures 3–5, PDF23 and 65–66

Question · Answer and explanation

Objective: aki-22, ckd-25

Pleuritic chest pain and a friction rub in advanced CKD require emergency assessment for pericarditis and other causes; suspected uremic pericarditis is an urgent dialysis indication. Other indications include refractory severe acidemia or hyperkalemia, pulmonary edema despite treatment, dialyzable poisoning and uremic encephalopathy. Severe hyperkalemia can require dialysis even without ECG changes.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — 5.4 Practice Points 1–3 and Table 41; 5.5 comprehensive conservative care

Question · Answer and explanation

Objective: ckd-09

The Kidney Failure Risk Equation (KFRE) estimates the chance that someone with CKD G3–G5 reaches kidney failure — dialysis or a transplant — within 2 and 5 years . KDIGO 2024 ties actions to it: a 5-year risk of 3–5% means refer to nephrology, a 2-year risk above 10% means multidisciplinary care, and above 40% means modality teaching and access and transplant preparation . It describes a group of people like her; it is not a countdown.

Source-supported decision rule; faculty review pending.

• Kidney Failure Risk Equation author calculator JavaScript — calculate_ckd_risk; calculate_2_year_ckd_risk; calculate_5_year_ckd_risk
• Tangri et al. multinational assessment of kidney failure risk equations — Methods, results and discussion
• KDIGO 2024 CKD guideline — Practice Points 2.2.1–2.2.3; Figure 48, printed S255 / PDF139

Question · Answer and explanation

Objective: ckd-21, ckd-09

An eGFR below 30 was already a KDIGO 2024 referral indication. The persistent A3 albuminuria and marked downward trend strengthen the need, and a reported 5-year KFRE of 25% is well above the 3–5% referral range. Do not label ACR above 300 alone or a fixed annual slope as the exact current KDIGO rule: its referral figure specifies combinations, higher albuminuria thresholds and other clinical circumstances. Earlier review would have allowed treatment optimization, vein preservation and time for education.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — Practice Points 2.2.1–2.2.3; Figure 48, printed S255 / PDF139

Question · Answer and explanation

Objective: ckd-25, ckd-22

Notice what did not change: her eGFR is still 17. The symptom that seemed to demand dialysis faded with medical treatment (correcting the acidosis, recovering from the infection and eating again may each have helped), and nothing else that would justify a start remains — no uremic symptom, no hyperkalemia, no acidosis, no fluid overload. Dialysis starts for symptoms or complications that treatment cannot control, and the IDEAL trial found no benefit from starting on the number ; her slope predicts a later start, not one today.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2024 CKD guideline — 5.4 Practice Points 1–3 and Table 41; 5.5 comprehensive conservative care
• KDIGO 2024 CKD guideline — 3.3.1 protein; 3.3.2 sodium; 3.10 acidosis

Question · Answer and explanation

Objective: ckd-22, ckd-24, ckd-09

G4 is the trigger for kidney-replacement teaching, and her slope and a one-in-three 2-year risk say now . Teach all five options in plain words — in-center hemodialysis, home hemodialysis, peritoneal dialysis, a pre-emptive transplant (before dialysis is ever needed, ideally from a living donor such as Mark) and conservative kidney management. Transplant evaluation starts at G4 so problems can be found and fixed — an active infection must be fully treated (hers is) and her heart will be checked — and access planning starts because a fistula needs months.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — Practice Points 2.2.1–2.2.3; Figure 48, printed S255 / PDF139
• KDIGO 2024 CKD guideline — 5.4 Practice Points 1–3 and Table 41; 5.5 comprehensive conservative care
• Kidney Failure Risk Equation author calculator JavaScript — calculate_ckd_risk; calculate_2_year_ckd_risk; calculate_5_year_ckd_risk

Question · Answer and explanation

Objective: ckd-23

A PICC may damage arm or central veins needed for future access. Preserve options in progressive CKD and involve the kidney/access team before another PICC. Prior left-arm instrumentation makes vascular mapping and an individualized access plan essential; neither automatic left-arm fistula creation nor automatic abandonment of that arm is justified. Timing should reflect progression risk, modality preference and the time required for maturation, not a single universal eGFR trigger.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2024 CKD guideline — 5.4 Practice Points 1–3 and Table 41; 5.5 comprehensive conservative care

Question · Answer and explanation

Objective: ckd-27

At G4 the target is about 0.8 g/kg of protein a day — 60 g for her — enough to protect muscle without a high-protein diet's acid and phosphate load; very-low-protein diets (about 0.3 g/kg with ketoanalogs) belong in specialist clinics that watch closely for malnutrition. Sodium under 2 g helps her pressure and ankles. Added phosphate — "PHOS" ingredients in deli meat, "enhanced" chicken, processed cheese and colas — is absorbed almost completely, so it goes first; potassium advice follows her labs, not a ban on produce.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — 3.3.1 protein; 3.3.2 sodium; 3.10 acidosis

Question · Answer and explanation

Objective: ckd-24, structural-25, structural-26

Conservative kidney management (CKM) is a planned choice to treat kidney failure without dialysis, and it is active care: symptoms, acidosis, anemia, potassium and fluid are still treated, an advance care plan is written, and palliative care joins . Its strongest candidates look like Agnes — very old, frail, with dementia and serious heart disease — while a robust 66-year-old who could receive a transplant should be prepared for one. Either plan is offered through a goals-of-care conversation built on what matters to the patient, never imposed.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — 5.4 Practice Points 1–3 and Table 41; 5.5 comprehensive conservative care

Question · Answer and explanation

Objective: ckd-04

Low muscle mass can cause creatinine-based eGFR to overestimate filtration. When a decision depends on greater precision, consider cystatin C and a combined creatinine–cystatin C estimate, while remembering that cystatin C also has non-GFR determinants. Serial results establish trajectory; one eGFR cannot show progression.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — Chapter 1 GFR evaluation and use of creatinine–cystatin C

Question · Answer and explanation

Objective: lytes-18

Healthy kidneys excrete extra magnesium so well that hypermagnesemia almost never happens with normal function; below an eGFR of 30, every magnesium laxative or antacid accumulates. Toxicity shows first as fading reflexes, then weakness, low blood pressure and slowed cardiac conduction. Polyethylene glycol holds water in the stool and adds no magnesium or phosphate; docusate and stimulant laxatives are the other alternatives.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2024 CKD guideline — Chapter 1 GFR evaluation and use of creatinine–cystatin C

Question · Answer and explanation

Objective: ckd-18, structural-18, structural-25

The apixaban label for atrial fibrillation lowers the dose to 2.5 mg twice daily when two of three are present — age 80 or older, weight 60 kg or less, creatinine 1.5 mg/dL or more (AF anticoagulation review §3.3) — and Walter meets all three. Dose by the label's own measure (here age, weight and creatinine; for other drugs, the renal metric specified by that product label), not by the eGFR on the portal. Whether to anticoagulate at all is a separate stroke-versus-bleeding decision.

Source-supported decision rule; faculty review pending.

• Apixaban prescribing information — 2.1 nonvalvular atrial fibrillation dosing

Question · Answer and explanation

Objective: htn-cardiorenal-04, structural-25

A systolic fall of 22 mmHg on standing, with symptoms, is orthostatic hypotension (a fall of 20 systolic or 10 diastolic within 3 minutes ), and in a frail 88-year-old the falls it causes outweigh a few mmHg of seated pressure. Over 80 the target is individualized — according to frailty, symptoms, standing pressure and patient priorities — and symptomatic orthostasis calls for less medication, not another drug. Amlodipine is the one to cut (to 5 mg, or held while he is this dry), with standing pressures at every visit.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2024 CKD guideline — Practice Points 3.6.2, 3.6.4, 3.6.5
• AHA/ACC 2025 high blood pressure guideline highlights — Items 4–10

Question · Answer and explanation

Objective: aki-27, lytes-14, lytes-18

An unexpected creatinine rise in clinic gets the same moves every time — repeat the chemistry, review drugs and intake, look at the urine, scan the bladder — then a choice between same-day care and a 48–72-hour recheck, made from the potassium, the ECG, the symptoms and the trajectory. Here a potassium of 6.1 comes with ECG changes and a rate of 46, the magnesium has taken his reflexes, and he was hypoglycemic an hour ago: each needs monitored treatment today . The clinic stops the culprits and hands him on.

Clinical application or calculation based on the cited principles; faculty review pending.

• UKKA adult hyperkalemia guideline, July 2026 update — Guidelines 16–17; 17.1.2 potassium monitoring; 17.2 glucose monitoring, PDF pp14 and 113–114

Question · Answer and explanation

Objective: lytes-13, lytes-18

IV calcium treats the hyperkalemic ECG changes and antagonizes magnesium's cardiac and neuromuscular effects. It lowers neither concentration. In parallel, stop the sources, use insulin with dextrose under close glucose surveillance to shift potassium, and arrange elimination. Correct volume depletion and use a loop only when urine output and volume assessment support it. Early nephrology review is appropriate for symptomatic hypermagnesemia with impaired renal clearance; refractory toxicity may need dialysis.

Clinical application or calculation based on the cited principles; faculty review pending.

• UKKA adult hyperkalemia guideline, July 2026 update — Guidelines 16–17; 17.1.2 potassium monitoring; 17.2 glucose monitoring, PDF pp14 and 113–114

Question · Answer and explanation

Objective: ckd-22, ckd-25

The serial results show little progression, and the creatinine change followed trimethoprim exposure, which can inhibit creatinine secretion. True AKI still requires assessment; the drug effect cannot be assumed to explain every rise. Symptoms improve as the acute electrolyte and drug problems are treated, so there is no demonstrated need to start dialysis during this admission. His CKD still warrants follow-up and goals-based planning. Either A or B can be justified; the learning target is the reduced likelihood of an immediate dialysis indication, not a validated distinction between the two labels.

Clinical application or calculation based on the cited principles; faculty review pending.

• Berglund et al. trimethoprim effect on serum creatinine and creatinine clearance — Abstract results
• KDIGO 2024 CKD guideline — 5.4 Practice Points 1–3 and Table 41; 5.5 comprehensive conservative care
• Kidney Failure Risk Equation author calculator JavaScript — calculate_ckd_risk; calculate_2_year_ckd_risk; calculate_5_year_ckd_risk

Question · Answer and explanation

Objective: structural-26, ckd-24, ckd-22

The surprise question is a screen the clinician asks privately; a "no" is a reason to talk, not a verdict. Ask Walter what he understands, fears and values most, recommend a plan that fits, and write it down. Conservative kidney management is that plan as active care — symptoms, potassium, acidosis, anemia and fluid still managed, palliative support when needed — and a planning referral at an eGFR under 30 fits inside it, because a referral is not a dialysis start.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — 5.4 Practice Points 1–3 and Table 41; 5.5 comprehensive conservative care

Question · Answer and explanation

Objective: lytes-01, structural-25

Orthostatic vital signs — a systolic fall of more than 20 mmHg (or diastolic more than 10) on standing — paired with a measured weight change (1 kg is about 1 L of fluid) are the most dependable bedside evidence that the circulation is short of volume. Signs built on skin and mucosa wear out with age.

Clinical application or calculation based on the cited principles; faculty review pending.

• NICE CG174 intravenous fluid therapy in adults — 1.1 assessment and monitoring; 1.3 resuscitation; 1.4 routine maintenance; 1.5 replacement and redistribution

Question · Answer and explanation

Objective: lytes-27

Thiazides block the sodium-chloride cotransporter in the distal convoluted tubule — the segment that dilutes urine — so they impair free-water excretion (low sodium), waste potassium and magnesium, and increase calcium reabsorption (high calcium) and uric acid retention. The first BMP (sodium, potassium, creatinine) belongs 1–2 weeks after starting or changing any diuretic, sooner and more often in older adults.

Clinical application or calculation based on the cited principles; faculty review pending.

• Lithium prescribing information — 5.1 lithium toxicity; 5.2 polyuria; drug interaction warnings

Question · Answer and explanation

Objective: lytes-02, lytes-10, aki-04

She is hypotensive with suspected AKI (creatinine twice an eight-month-old baseline, so the timing needed for formal staging is not yet established), so the circulation comes first — and to a plasma sodium of 157, 0.9% saline (154 mEq/L) is effectively isotonic: (154 − 157) ÷ (27 + 1) ≈ −0.1 mEq/L per liter. Then free water: deficit = total body water × (Na/140 − 1) = (0.45 × 60) × (157/140 − 1) = 27 × 0.121 ≈ 3.3 L, plus ongoing urine and insensible losses, given as D5W or water by mouth when safe. For hypernatremia of uncertain duration, use an initially conservative correction plan of about 10 mEq/L over 24 hours, adjust to serial sodium and ongoing losses, and avoid prolonged undercorrection. The traditional 10–12 mEq/L daily limit is not a proven universal adult safety boundary; adult observational evidence is conflicting and does not establish an optimal rate.

Clinical application or calculation based on the cited principles; faculty review pending.

• NICE CG174 intravenous fluid therapy in adults — 1.1 assessment and monitoring; 1.3 resuscitation; 1.4 routine maintenance; 1.5 replacement and redistribution
• Feigin et al. rate of correction and mortality in severe adult hypernatremia — Abstract methods and results

Question · Answer and explanation

Objective: lytes-10

If no water going in were the whole story, ADH would be at full strength — her serum osmolality is 337 — and a kidney that can respond would make concentrated urine, above 600 mOsm/kg. Urine at 160 with a sodium of 157 is a kidney pouring out free water during a water deficit: diabetes insipidus. The finding counts only because it is paired with the high sodium; 160 in someone with a sodium of 138 who just drank water would be normal.

Clinical application or calculation based on the cited principles; faculty review pending.

• Lithium prescribing information — 5.1 lithium toxicity; 5.2 polyuria; drug interaction warnings

Question · Answer and explanation

Objective: lytes-10, structural-22

A rise from 160 to 172 is only 7.5%, indicating little concentrating response to desmopressin in this patient with persistent hypernatremia. Long lithium exposure strongly supports nephrogenic diabetes insipidus; hypercalcemia can further impair concentration. Response cutoffs overlap in partial disorders and chronic polyuria, so the percentage is interpreted with the clinical context rather than as an infallible binary test.

Clinical application or calculation based on the cited principles; faculty review pending.

• Lithium prescribing information — 5.1 lithium toxicity; 5.2 polyuria; drug interaction warnings

Question · Answer and explanation

Objective: lytes-15, lytes-27

The PTH is inappropriately unsuppressed for hypercalcemia, supporting a PTH-dependent process such as lithium-associated hyperparathyroidism; the thiazide may contribute. Rehydrate, hold contributing drugs and confirm calcium status, using ionized calcium if needed. Clinical severity, not a calcium cutoff alone, determines urgent escalation. Bisphosphonates are not a routine first response to this suspected mechanism; treatment choice in kidney dysfunction is individualized rather than governed by a universal ban at CrCl 30.

Clinical application or calculation based on the cited principles; faculty review pending.

• Society for Endocrinology emergency management of acute hypercalcemia — Investigations and management sections
• Lithium prescribing information — 5.1 lithium toxicity; 5.2 polyuria; drug interaction warnings

Question · Answer and explanation

Objective: aki-13, structural-20, structural-22

Keep the interacting drugs held while recovery and the long-term psychiatric plan are assessed. A lithium level back in range does not by itself establish neurologic recovery or make the old regimen safe. Earlier, her persistent decreased consciousness justified urgent extracorporeal treatment under EXTRIP recommendations regardless of the modest serum concentration. After treatment, follow serial lithium levels for rebound, electrolytes and neurologic findings with toxicology/nephrology. Psychiatry and nephrology jointly plan mood treatment and any eventual lithium restart; do not automatically restart because one level is low.

Source-supported decision rule; faculty review pending.

• EXTRIP lithium recommendations — Indications for extracorporeal treatment; cessation and monitoring
• Lithium prescribing information — 5.1 lithium toxicity; 5.2 polyuria; drug interaction warnings
• NICE CG185 bipolar disorder: using lithium — 1.10.14–1.10.23

Question · Answer and explanation

Objective: structural-22, ckd-21

Lithium-associated concentrating defects and chronic tubulointerstitial injury are related but different problems. A sustained eGFR decline warrants evaluation for other causes and a joint renal–psychiatric risk–benefit discussion. One current lithium level does not summarize years of exposure, and abrupt unplanned psychiatric treatment changes can cause harm.

Clinical application or calculation based on the cited principles; faculty review pending.

• NICE CG185 bipolar disorder: using lithium — 1.10.14–1.10.23
• KDIGO 2024 CKD guideline — Practice Points 2.2.1–2.2.3; Figure 48, printed S255 / PDF139

Question · Answer and explanation

Objective: lytes-02

Dextrose is metabolized within minutes, so what stays in the body is the bag's salt and water. D5 ½NS carries 77 mEq/L of sodium — half of 0.9% saline — so about half of every liter is free water. After surgery, pain, nausea, opioids and stress switch ADH on, the kidney keeps that water, and the sodium falls: hospital-acquired hyponatremia.

Source-supported decision rule; faculty review pending.

• NICE CG174 intravenous fluid therapy in adults — 1.1 assessment and monitoring; 1.3 resuscitation; 1.4 routine maintenance; 1.5 replacement and redistribution

Question · Answer and explanation

Objective: lytes-09

Brain cells adapt to a low sodium over about 48 hours by shedding solutes so that they do not swell. A sodium that falls faster than that swells the brain, so acute hyponatremia seizes at numbers a slowly adapted brain tolerates. The flip side: the adapted brain is the one injured by fast correction (osmotic demyelination), which is why the correction ceiling applies once hyponatremia has lasted more than 48 hours, or no one knows how long.

Clinical application or calculation based on the cited principles; faculty review pending.

• European clinical practice guideline on hyponatremia — 7.1.1.1–7.1.1.4 severe symptoms; 7.2 moderately severe symptoms

Question · Answer and explanation

Objective: lytes-01, lytes-04, lytes-05

Measured serum osmolality confirms hypotonic hyponatremia. Concentrated urine despite hypotonic plasma indicates antidiuretic activity; the examination, urine sodium and low BUN/urate support a postoperative SIADH pattern after assessing thyroid, adrenal and renal function. Hypotonic intake plus pain, nausea and medicines provide plausible contributors. Sodium depends on both water and exchangeable sodium/potassium balance; the available intake and weight data cannot establish an exact retained free-water volume.

Clinical application or calculation based on the cited principles; faculty review pending.

• European clinical practice guideline on hyponatremia — 7.1.1.1–7.1.1.4 severe symptoms; 7.2 moderately severe symptoms
• NICE CG174 intravenous fluid therapy in adults — 1.1 assessment and monitoring; 1.3 resuscitation; 1.4 routine maintenance; 1.5 replacement and redistribution

Question · Answer and explanation

Objective: lytes-02, lytes-05, lytes-12

Stop the hypotonic fluid and ketorolac, restrict further free water and obtain urgent senior review of the neurologic symptoms. A single 150-mL 3% bolus is guideline-supported for moderately severe symptoms attributable to hyponatremia; severe deterioration requires emergency bolus treatment. Recheck sodium promptly and use the correction limits in Q7. Repeat the hemolyzed potassium immediately: the normal ECG does not exclude hyperkalemia, but this discordant specimen needs rapid confirmation while the patient is monitored.

Clinical application or calculation based on the cited principles; faculty review pending.

• European clinical practice guideline on hyponatremia — 7.1.1.1–7.1.1.4 severe symptoms; 7.2 moderately severe symptoms
• NICE CG174 intravenous fluid therapy in adults — 1.1 assessment and monitoring; 1.3 resuscitation; 1.4 routine maintenance; 1.5 replacement and redistribution

Question · Answer and explanation

Objective: lytes-05

The fall after saline weakens volume depletion as the main explanation and supports persistent antidiuresis in this context. Isotonic saline can worsen SIADH when sodium and potassium are excreted in urine sufficiently concentrated relative to plasma, leaving retained electrolyte-free water. Total urine osmolality alone cannot quantify that effect because it includes urea; urine sodium plus potassium and measured balances are needed. The observed response is evidence, not a universal diagnostic test.

Clinical application or calculation based on the cited principles; faculty review pending.

• European clinical practice guideline on hyponatremia — 7.1.1.1–7.1.1.4 severe symptoms; 7.2 moderately severe symptoms

Question · Answer and explanation

Objective: lytes-08

A seizure requires emergency hypertonic saline with close monitoring. This case uses the European protocol: 150 mL of 3% saline over 20 minutes, reassess symptoms and sodium, and repeat as needed up to three boluses total to obtain about a 5 mEq/L early rise. Stop rescue boluses when the immediate target is achieved and follow correction limits. A closed-system estimate predicts about 1.9 mEq/L per bolus here, but ongoing urine losses and other fluids can make the actual change very different; measure rather than dose to the formula.

Source-supported decision rule; faculty review pending.

• European clinical practice guideline on hyponatremia — 7.1.1.1–7.1.1.4 severe symptoms; 7.2 moderately severe symptoms

Question · Answer and explanation

Objective: lytes-09

Her hyponatremia has lasted more than 48 hours (131 on Tuesday at 06:00, 49 hours before the seizure), so her brain has begun to adapt and the ceiling applies: no more than 8 mEq/L in 24 hours, never more than 10. She is at +7 with 17 hours to run. With the ADH stimuli gone, dilute urine at 260 mL/h is a water diuresis that can add 10 or more by morning; slowing it (D5W, sometimes desmopressin) is nephrology's call, made before the ceiling is crossed.

Clinical application or calculation based on the cited principles; faculty review pending.

• European clinical practice guideline on hyponatremia — 7.1.1.1–7.1.1.4 severe symptoms; 7.2 moderately severe symptoms

Question · Answer and explanation

Objective: structural-01

Non-contrast CT is the first-line test: it detects most stone types — including the uric acid stones a plain film misses — gives size and location, shows hydronephrosis, and finds the alternatives such as an aortic aneurysm. No contrast is needed, and a low-dose stone protocol limits the radiation. Ultrasound is the choice in pregnancy, so a woman of reproductive age has a pregnancy test first.

Source-supported decision rule; faculty review pending.

• EAU Urolithiasis guideline — 3.3 Diagnostic evaluation; imaging

Question · Answer and explanation

Objective: lytes-23

The urine anion gap is (30 + 25) − 85 = −30. In this non-gap acidosis, a negative gap is consistent with increased ammonium excretion, often as ammonium chloride, and supports an appropriate renal response to diarrhea. It is an indirect index: unusual urinary anions, low distal sodium delivery and bicarbonaturia can make it misleading. A negative gap does not exclude proximal RTA; direct urine ammonium is preferable when available and the distinction remains uncertain.

Clinical application or calculation based on the cited principles; faculty review pending.

• Batlle et al. urine anion gap and hyperchloremic acidosis — Abstract methods and results

Question · Answer and explanation

Objective: lytes-23

A pH of 7.33 with a bicarbonate of 17 is a metabolic acidosis. The anion gap is 139 − (114 + 17) = 8 (normal 8–12), so it is non-gap (hyperchloremic), and Winter's formula, 1.5 × 17 + 8 = 33.5 ± 2, matches her pCO₂ of 33 — one disorder, properly compensated. A non-gap acidosis has two homes, the gut and the kidney, and the urine anion gap, from electrolytes added to the triage urine collected before any IV fluid, helps distinguish them, while direct urine ammonium and the full clinical context can resolve uncertainty.

Clinical application or calculation based on the cited principles; faculty review pending.

• Batlle et al. urine anion gap and hyperchloremic acidosis — Abstract methods and results
• EAU metabolic evaluation and recurrence prevention — 4.6.5 renal tubular acidosis

Question · Answer and explanation

Objective: lytes-23, lytes-24

The positive urine anion gap during systemic acidosis suggests an inadequate ammonium response, weakening diarrhea as the main explanation. The alkaline urine, recurrent calcium phosphate stones and nephrocalcinosis make a distal acidification disorder more coherent. The gap is a proxy, not a measured ammonium concentration; review confounders and use direct ammonium or specialist testing if findings are discordant. Diarrhea may still contribute.

Clinical application or calculation based on the cited principles; faculty review pending.

• EAU metabolic evaluation and recurrence prevention — 4.6.5 renal tubular acidosis
• Batlle et al. urine anion gap and hyperchloremic acidosis — Abstract methods and results

Question · Answer and explanation

Objective: lytes-24, structural-03

A low potassium, a urine pH above 5.5 during acidemia, a positive urine anion gap, and calcium phosphate stones with nephrocalcinosis add up to type 1 (distal) RTA: the collecting duct cannot pump acid into the urine, so it cannot acidify, it wastes potassium, and its alkaline, citrate-poor, calcium-rich urine grows calcium phosphate. Sjögren syndrome is an important acquired cause in an adult with sicca symptoms; her dry eyes, dry mouth, gumline cavities and parotid swelling are the clue, so the screen is ANA, anti-Ro/SSA, anti-La/SSB and rheumatoid factor.

Clinical application or calculation based on the cited principles; faculty review pending.

• EAU metabolic evaluation and recurrence prevention — 4.6.5 renal tubular acidosis

Question · Answer and explanation

Objective: lytes-11, structural-03

Potassium citrate replaces the potassium the tubule wastes, becomes bicarbonate, and raises urine citrate, a stone inhibitor — and it delivers the potassium with the alkali, which matters because raising the blood pH drives potassium into cells. The stone lecture calls citrate double-edged in calcium phosphate disease since alkali raises urine pH, but in distal RTA the urine is already alkaline from the defect and correcting the acidosis lowers urine calcium — so the RTA sources prefer it, with urine pH rechecked. Fluids, low salt and normal calcium complete the plan.

Source-supported decision rule; faculty review pending.

• Potassium citrate extended-release prescribing information — 2.1 monitoring; 2.2 severe hypocitraturia
• EAU metabolic evaluation and recurrence prevention — 4.6.5 renal tubular acidosis
• EAU metabolic evaluation and recurrence prevention — 4.1.2 urine sampling; 4.2 general preventive measures

Question · Answer and explanation

Objective: htn-cardiorenal-03

Average the readings first: 136/91. Stage 1 is a systolic of 130–139 or a diastolic of 80–89; stage 2 is a systolic of 140 or more or a diastolic of 90 or more. When the two numbers land in different categories, the higher category sets the stage, so a diastolic of 91 makes this stage 2.

Source-supported decision rule; faculty review pending.

• 2025 AHA/ACC adult high blood pressure guideline — BP measurement/classification and treatment recommendations; §5.1 Table 12

Question · Answer and explanation

Objective: htn-cardiorenal-05

Five kilograms × roughly 1 mmHg/kg gives an estimated 5-mmHg systolic reduction. This is an average expectation, not a promise or a reason to stop treatment before measuring the response; diet, exercise and sodium reduction can also help, but their effects should not be added as guaranteed independent benefits.

Source-supported decision rule; faculty review pending.

• 2025 AHA/ACC adult high blood pressure guideline — BP measurement/classification and treatment recommendations; §5.1 Table 12

Question · Answer and explanation

Objective: htn-cardiorenal-02, htn-cardiorenal-14

A mean of 144/91 is stage 2 by office criteria, and confirmed stage 2 is treated at once with two drugs — but one visit is not yet a diagnosis. An office pressure of 130–159/80–99 is the band in which white-coat hypertension (15–30% of high office readings) must be excluded with home or ambulatory readings, and two of his medicines raise pressure: pseudoephedrine constricts arterioles, naproxen retains salt and water. Remove them (saline or steroid nasal spray; acetaminophen or topical diclofenac for golf) and measure what is left.

Source-supported decision rule; faculty review pending.

• 2025 AHA/ACC adult high blood pressure guideline — BP measurement/classification and treatment recommendations; §5.1 Table 12
• Endocrine Society Primary Aldosteronism guideline 2025 — Recommendations 1 and 3, screening technical remarks and medication-interference strategy

Question · Answer and explanation

Objective: htn-cardiorenal-06, htn-cardiorenal-07

Confirmed stage 2 hypertension supports two first-line agents. An ACE inhibitor is a reasonable choice with albuminuria, which must be repeated to establish CKD; a thiazide-like diuretic can be a partner. Review the pending potassium before starting either drug and repeat renal function and electrolytes within 1–2 weeks of initiation or dose change in this patient.

Source-supported decision rule; faculty review pending.

• 2025 AHA/ACC adult high blood pressure guideline — BP measurement/classification and treatment recommendations; §5.1 Table 12
• KDIGO 2024 CKD guideline — Tables 1–3 (S137); §4.2 PP4.2.5; §4.3 PP4.3.1–4.3.3; Figure 47; §1.3.1/PP1.3.1.4, S192–193 (first-morning urine and orthostatic proteinuria)

Question · Answer and explanation

Objective: htn-cardiorenal-11

Spontaneous hypokalemia with alkalosis raises concern for primary aldosteronism, so uncomplicated primary hypertension is less satisfactory as the only explanation. Diuretic-associated hypokalemia also supports screening; it should not be dismissed or assigned an arbitrary potassium threshold. Correct potassium and review interfering medicines before interpreting the aldosterone–renin ratio.

Clinical application or calculation based on the cited principles; faculty review pending.

• Endocrine Society Primary Aldosteronism guideline 2025 — Recommendations 1 and 3, screening technical remarks and medication-interference strategy

Question · Answer and explanation

Objective: lytes-27, ckd-11

Spironolactone blocks the aldosterone receptor in the collecting duct, so the kidney stops spending potassium. Its signature is the mirror image of the thiazide's (potassium rises instead of falling), and stacked on an ACE inhibitor, which lowers aldosterone, plus a potassium supplement, it sets up hyperkalemia. The supplement stops the day the MRA starts; potassium and creatinine are checked within about a week, then monthly at first.

Source-supported decision rule; faculty review pending.

• ALDACTONE prescribing information — §5.1 and §7.1

Question · Answer and explanation

Objective: ckd-01, ckd-02, ckd-03

CKD is an abnormality of kidney structure or function lasting more than 3 months — a GFR below 60 or a marker of damage such as albuminuria of 30 mg/g or more . His only eGFR under 60 was a single value drawn on naproxen and never repeated, so G3a was never established. His UACR has stayed at 30 mg/g or above on samples more than 3 months apart: CKD by albuminuria with a preserved eGFR — G2 A2, yellow on the KDIGO heat map (moderately increased risk), cause hypertension with primary aldosteronism.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — Tables 1–3 (S137); §4.2 PP4.2.5; §4.3 PP4.3.1–4.3.3; Figure 47; §1.3.1/PP1.3.1.4, S192–193 (first-morning urine and orthostatic proteinuria)

Question · Answer and explanation

Objective: htn-cardiorenal-27

CKM describes interacting metabolic, cardiovascular and kidney risks. Blood pressure, adiposity, glycemia, albuminuria and kidney function should inform one prevention plan, with lifestyle treatment and indicated medicines selected for the individual. CKM framing complements CKD staging and cardiovascular risk assessment; it does not replace either.

Source-supported decision rule; faculty review pending.

• 2026 AHA/ACC cardiovascular-kidney-metabolic syndrome guideline — §2.3 and §5.1, Figure 5

Question · Answer and explanation

Objective: structural-18, ckd-18

The gabapentin label describes Cockcroft–Gault estimation of creatinine clearance in stable kidney function. Use the estimate and patient characteristics specified by each drug label: metformin uses eGFR, while apixaban for atrial fibrillation uses its own age, weight and creatinine criteria. No single dosing rule applies to every medicine.

Source-supported decision rule; faculty review pending.

• NEURONTIN prescribing information — §2.3 Table 1 and Cockcroft–Gault equation; §2.5

Question · Answer and explanation

Objective: aki-13, structural-19, structural-20

Each drug removes one of the kidney's defenses of filtration when volume falls: the diuretic lowers volume, the ACE inhibitor or ARB removes the angiotensin squeeze on the outflow (efferent) arteriole that holds glomerular pressure up, and the NSAID removes the prostaglandin dilation of the inflow (afferent) arteriole. Risk depends on the patient and the clinical state; even two can be hazardous during volume depletion. The three-drug combination is particularly concerning.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — Tables 1–3 (S137); §4.2 PP4.2.5; §4.3 PP4.3.1–4.3.3; Figure 47; §1.3.1/PP1.3.1.4, S192–193 (first-morning urine and orthostatic proteinuria)

Question · Answer and explanation

Objective: structural-18, ckd-18

Cockcroft–Gault gives (140 − 74) × 80 / (72 × 2.7) = 27.2 mL/min. For nonvalvular atrial fibrillation, the US rivaroxaban label uses 15 mg once daily with the evening meal when CrCl is 50 or below. Patients below 30 were not enrolled in the pivotal AF trial, so this advanced-CKD patient needs an individualized anticoagulation review and close bleeding/kidney monitoring.

Source-supported decision rule; faculty review pending.

• XARELTO prescribing information — §2.1 Table 1 and renal-function footnotes

Question · Answer and explanation

Objective: structural-18, structural-19, structural-23, ckd-18

Stop metformin at eGFR below 30 and stop oral naproxen. His CrCl is approximately 27 mL/min: gabapentin 2,700 mg/day is excessive and likely contributes to sedation and falls. Its label range at CrCl >15–29 is 200–700 mg once daily; 300 mg nightly is a cautious patient-specific proposal, not the ceiling for all patients below eGFR 30. Assess toxicity promptly and individualize holding/reduction and withdrawal precautions with the prescriber; reassess whether gabapentin is still needed.

Source-supported decision rule; faculty review pending.

• NEURONTIN prescribing information — §2.3 Table 1 and Cockcroft–Gault equation; §2.5
• Metformin prescribing information — §2.3 renal impairment and §2.4 iodinated contrast
• KDIGO 2024 CKD guideline — Tables 1–3 (S137); §4.2 PP4.2.5; §4.3 PP4.3.1–4.3.3; Figure 47; §1.3.1/PP1.3.1.4, S192–193 (first-morning urine and orthostatic proteinuria)

Question · Answer and explanation

Objective: structural-15, structural-19

Oral sodium phosphate can cause acute phosphate nephropathy — calcium phosphate deposits in the tubules, often permanent — and it is avoided in CKD of any stage and in older patients on an ARB or a diuretic; all four describe him , so polyethylene glycol is the prep. The gadolinium agents that caused nephrogenic systemic fibrosis were group I; group II agents have a very low NSF risk. When MRI contrast is clinically needed, radiology uses a group II agent at a dose sufficient for diagnosis; reducing below diagnostic quality is not a safety strategy.

Source-supported decision rule; faculty review pending.

• OsmoPrep FDA prescribing information — Boxed warning: acute phosphate nephropathy; warnings renal disease
• ACR Manual on Contrast Media 2026 — Metformin pp48–49 Category I/II; CA-AKI pp43–44; NSF pp80–82

Question · Answer and explanation

Objective: lytes-18

Magnesium normalized after PPI withdrawal without taking the supplement, while the reported diet and diuretic were unchanged. That dechallenge makes a PPI contribution more likely and a diet-only explanation less convincing. It does not prove one exclusive cause or a specific molecular mechanism; ongoing follow-up checks that the response persists.

Clinical application or calculation based on the cited principles; faculty review pending.

• Omeprazole prescribing information — Warnings and precautions: hypomagnesemia and mineral metabolism

Question · Answer and explanation

Objective: ckd-20, aki-15, htn-cardiorenal-25, structural-19

The written plan temporarily holds medicines that can worsen dehydration-related kidney problems or ketoacidosis risk. CKD G4 and rivaroxaban make prompt clinical advice important: inability to take the anticoagulant with food, bleeding, hypotension or suspected AKI requires individualized review. Do not stop beta-blockers or anticoagulation reflexively, double missed doses, or restart all held drugs automatically; document recovery, laboratory assessment when indicated and the restart plan.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — Tables 1–3 (S137); §4.2 PP4.2.5; §4.3 PP4.3.1–4.3.3; Figure 47; §1.3.1/PP1.3.1.4, S192–193 (first-morning urine and orthostatic proteinuria)
• XARELTO prescribing information — §2.1 Table 1 and renal-function footnotes

Question · Answer and explanation

Objective: lytes-18

Reduced kidney clearance allows magnesium to accumulate. Neuromuscular depression and bradycardia are warning signs of toxicity, so stop the source and arrange urgent monitored care. Severe cases may need IV calcium for physiologic antagonism and dialysis for removal; those decisions depend on symptoms, ECG and kidney function.

Source-supported decision rule; faculty review pending.

• Magnesium sulfate prescribing information — Warnings and Overdosage
• KDIGO 2012 AKI guideline (current final guideline; 2026 draft not final) — §2.1.1–2/Table2; §2.3.4; §3.8.1–4; §5.1.1–2

Question · Answer and explanation

Objective: glom-07

Nephrotic syndrome is a leak: the glomerular filter loses so much protein (more than 3.5 g a day) that serum albumin falls below 3.0 g/dL, oncotic pressure falls and edema follows, while the liver's response drives cholesterol up. Oval fat bodies and fatty casts are its urine signature. Nephritic syndrome is inflammation: hematuria with red-cell casts, hypertension and a falling GFR, with less protein.

Source-supported decision rule; faculty review pending.

• KDIGO 2021 Glomerular Diseases guideline with 2024 lupus update — PP1.3.1 urine sediment; PP1.4.1–1.4.5 edema; PP3.1.1–3.1.2 membranous diagnosis and associated-cause evaluation

Question · Answer and explanation

Objective: glom-24

Hydralazine, like propylthiouracil and levamisole-cut cocaine, can trigger ANCA vasculitis, and stopping the drug is part of the treatment. The rest of the student table: NSAIDs → minimal change disease, membranous nephropathy and interstitial nephritis; lithium → FSGS or minimal change disease (and nephrogenic diabetes insipidus); pamidronate → FSGS, often the collapsing form.

Source-supported decision rule; faculty review pending.

• Kumar et al. Hydralazine-associated vasculitis, 2018 — Abstract: Introduction, Methods, Results and Conclusions

Question · Answer and explanation

Objective: glom-20

Before a third diuretic, find the cause of the edema. Generalized edema comes from high capillary pressure (a failing heart or blocked veins) or low oncotic pressure (albumin lost through the kidney or not made by the liver), and the bedside already leans away from the heart: normal neck veins, clear lungs, no S3, periorbital swelling that is worst in the morning. A urinalysis with microscopy, a protein-to-creatinine ratio and a serum albumin test the kidney; a BNP tests the heart. A basic metabolic panel does not include albumin, which is how this gets missed.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2021 Glomerular Diseases guideline with 2024 lupus update — PP1.3.1 urine sediment; PP1.4.1–1.4.5 edema; PP3.1.1–3.1.2 membranous diagnosis and associated-cause evaluation

Question · Answer and explanation

Objective: glom-07, glom-20

The very heavy proteinuria provides a compelling renal explanation for edema, while the low BNP reduces the likelihood of decompensated heart failure. BNP is influenced by treatment and patient factors and does not independently exclude heart failure; the subsequent echocardiogram adds information. The combination shifts the leading diagnosis toward nephrotic disease.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2021 Glomerular Diseases guideline with 2024 lupus update — PP1.3.1 urine sediment; PP1.4.1–1.4.5 edema; PP3.1.1–3.1.2 membranous diagnosis and associated-cause evaluation

Question · Answer and explanation

Objective: lytes-07, glom-21, structural-20

His hyponatremia is hypervolemic — water held by ADH (urine osmolality 420) in a body already overloaded with salt and water — so it is treated with the edema: sodium restriction, a modest fluid limit and a loop diuretic dosed for a nephrotic kidney. Low albumin delivers less furosemide to the tubule and a swollen gut absorbs less, so the dose rises and is split; naproxen goes because it blunts the diuretic and is contraindicated in nephrotic syndrome. A proposed loss of 0.5–1 kg/day requires daily weights, perfusion assessment and electrolyte/creatinine checks; the rate must slow if underfilling develops.

Source-supported decision rule; faculty review pending.

• KDIGO 2021 Glomerular Diseases guideline with 2024 lupus update — PP1.3.1 urine sediment; PP1.4.1–1.4.5 edema; PP3.1.1–3.1.2 membranous diagnosis and associated-cause evaluation
• KDIGO 2024 CKD guideline — Tables 1–3 (S137); §4.2 PP4.2.5; §4.3 PP4.3.1–4.3.3; Figure 47; §1.3.1/PP1.3.1.4, S192–193 (first-morning urine and orthostatic proteinuria)

Question · Answer and explanation

Objective: glom-10, glom-18

Anti-PLA2R with this nephrotic presentation supports PLA2R-associated membranous nephropathy and may allow diagnosis without biopsy. KDIGO still calls for evaluation of associated conditions regardless of antibody status; a positive result does not exclude cancer, infection or a coincident drug contribution. Stop naproxen and let nephrology assess disease risk, biopsy value and treatment.

Source-supported decision rule; faculty review pending.

• KDIGO 2021 Glomerular Diseases guideline with 2024 lupus update — PP1.3.1 urine sediment; PP1.4.1–1.4.5 edema; PP3.1.1–3.1.2 membranous diagnosis and associated-cause evaluation

Question · Answer and explanation

Objective: glom-19

The nephrotic state, marked hypoalbuminemia, flank pain, hematuria and acute creatinine rise make renal vein thrombosis an urgent concern. Arrange appropriate vascular imaging and contact nephrology the same day. An empty bladder argues against lower-tract retention but does not exclude upper-tract obstruction; no pyuria does not rule out AIN. Reassess perfusion, drugs and obstruction alongside the leading vascular diagnosis, rather than treating single negative findings as exclusions.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2021 Glomerular Diseases guideline with 2024 lupus update — PP1.3.1 urine sediment; PP1.4.1–1.4.5 edema; PP3.1.1–3.1.2 membranous diagnosis and associated-cause evaluation
• KDIGO 2012 AKI guideline (current final guideline; 2026 draft not final) — §2.1.1–2/Table2; §2.3.4; §3.8.1–4; §5.1.1–2

Question · Answer and explanation

Objective: htn-cardiorenal-17

Under 13, blood pressure is read against age, sex and height, because taller children normally run higher pressures. Both of his numbers sit at or above the 95th percentile (112 ≥ 108, 70 ≥ 66) and below the 95th + 12 line (120/78): the stage 1 range, which becomes a diagnosis only after elevated readings on three occasions. It matters in this case because a normal blood pressure is one of the features that makes childhood nephrotic syndrome typical.

Source-supported decision rule; faculty review pending.

• AAP pediatric hypertension guideline — Table 3 category definitions and §4.3c ABPM
• AAP Table 4 reproduced by Connecticut Children's — Appendix G, PDF page1: boys age4 and age7, 50th-height column
• AAP 2017 hypertension guideline correction — Correction text
• AAP 2018 hypertension guideline correction — Correction text

Question · Answer and explanation

Objective: glom-04

A child loses far less protein in absolute terms than an adult, so the pediatric line is scaled to body size: at least 1,000 mg/m²/day on a timed collection, or a spot UPCR of at least 2 g/g. For a 4-year-old (about 0.75 m²) that is roughly 0.75 g a day, so he can be profoundly nephrotic — anasarca, a very low albumin — well below the adult 3.5 g. Low albumin, edema and high cholesterol complete the syndrome at any age.

Source-supported decision rule; faculty review pending.

• KDIGO 2025 Nephrotic Syndrome in Children guideline — S262–263/Figure 1 definitions; PP1.2.1/Figure 2 biopsy indications; Recommendation1.3.1.1

Question · Answer and explanation

Objective: glom-08, glom-23

His typical childhood nephrotic presentation supports initial oral glucocorticoids under pediatric nephrology without routine biopsy. This predicts steroid sensitivity; it does not prove minimal-change histology. Sustained hypertension, gross hematuria, low complement, AKI not explained by hypovolemia, syndromic features or steroid resistance prompt reconsideration; the NSAID exposure is removed but does not by itself establish causation.

Source-supported decision rule; faculty review pending.

• KDIGO 2025 Nephrotic Syndrome in Children guideline — S262–263/Figure 1 definitions; PP1.2.1/Figure 2 biopsy indications; Recommendation1.3.1.1

Question · Answer and explanation

Objective: glom-19

A nephrotic child loses immunoglobulins and complement factors in the urine, which leaves him at increased risk of invasive bacterial infection, including pneumococcus, and he is on prednisone besides. Fever with diffuse abdominal tenderness in a child with ascites is bacterial peritonitis until cultures say otherwise: a same-night emergency. The same urine losses explain the other big complication — antithrombin and protein S go out while the liver makes more fibrinogen, so nephrotic children clot, which is one more reason not to over-diurese.

Clinical application or calculation based on the cited principles; faculty review pending.

• Royal Children’s Hospital Nephrotic syndrome guideline, July 2025 — Significant complications; investigations; treatment and nephrology consultation

Question · Answer and explanation

Objective: glom-09, glom-18, glom-23

FSGS is a scar pattern: the same lesion comes from a primary podocyte disease or from injury by obesity, HIV, heroin, pamidronate or low nephron mass, and treatment depends on the cause; empiric steroids should not precede this evaluation. So every adult with new nephrotic syndrome gets the secondary-cause screen — HIV, hepatitis B and C, syphilis, ANA, complements, A1c, protein electrophoresis with free light chains — and an ultrasound before treatment; biopsy is nephrology's call after that. His weight is a weak explanation: obesity-related FSGS usually spares the albumin and the edema, and he has the full syndrome.

Source-supported decision rule; faculty review pending.

• KDIGO 2021 Glomerular Diseases guideline with 2024 lupus update — PP1.3.1 urine sediment; PP1.4.1–1.4.5 edema; PP3.1.1–3.1.2 membranous diagnosis and associated-cause evaluation
• HIVMA/IDSA CKD guideline — III recommendations1–3; IV1; evidence discussion of HIVAN and biopsy

Question · Answer and explanation

Objective: glom-09, glom-25

Uncontrolled HIV with nephrotic proteinuria and enlarged echogenic kidneys strongly raises concern for HIV-associated nephropathy. Kidney size and echogenicity are nonspecific, and HIV can accompany other kidney lesions; biopsy may be needed. The finding shifts the working explanation away from an assumed primary FSGS, while treatment of HIV should begin promptly.

Clinical application or calculation based on the cited principles; faculty review pending.

• HIVMA/IDSA CKD guideline — III recommendations1–3; IV1; evidence discussion of HIVAN and biopsy

Question · Answer and explanation

Objective: glom-25, glom-22

HIVAN is driven by virus inside the podocytes, so the treatment is viral suppression: antiretroviral therapy started promptly, to suppress the virus and reduce progression risk; kidney recovery varies. The ACE inhibitor adds protein reduction and BP control; with a potassium of 4.9 and a creatinine of 1.9, both are rechecked within 1–2 weeks. Nephrology decides whether to biopsy — it can confirm HIVAN and exclude an HIV-related immune-complex GN — but the antiretrovirals do not wait for it.

Source-supported decision rule; faculty review pending.

• HIVMA/IDSA CKD guideline — III recommendations1–3; IV1; evidence discussion of HIVAN and biopsy
• KDIGO 2024 CKD guideline — Tables 1–3 (S137); §4.2 PP4.2.5; §4.3 PP4.3.1–4.3.3; Figure 47; §1.3.1/PP1.3.1.4, S192–193 (first-morning urine and orthostatic proteinuria)

Question · Answer and explanation

Objective: glom-17

Both antibodies are made against streptococcal products, but after a skin infection anti-DNase B is the more sensitive marker; ASO is the better marker after a sore throat. A rising titer on the repeat sample is more convincing than a single value — the ASO, for example, peaks 3–5 weeks after the infection. By the time the kidney flares the organism is usually long gone, which is why antibodies, not swabs, carry the history.

Source-supported decision rule; faculty review pending.

• Kaplan et al., immune response to streptococcal infections 1970 — Abstract, skin versus upper-respiratory infection antibody responses
• CDC Clinical Guidance for PSGN — Diagnosis, Treatment and Prognosis

Question · Answer and explanation

Objective: glom-12

Purpura you can feel, on dependent skin, with joint pain, abdominal pain and kidney involvement is the tetrad of IgA vasculitis — inflamed small vessels, not a shortage of platelets, so the count is normal. It peaks between ages 2 and 15, the kidney is involved in about 40–50% of children, and complement stays normal, which separates it from post-streptococcal GN. Its kidney lesion is the same IgA deposit seen in IgA nephropathy.

Source-supported decision rule; faculty review pending.

• IPNA recommendations for children with IgA nephropathy and IgA vasculitis nephritis — IgAVN diagnosis/workup, recommendations1a and1b and differential table

Question · Answer and explanation

Objective: glom-07, htn-cardiorenal-17

Blood in the urine, less urine, new swelling and a high BP are the nephritic pattern — an inflamed glomerulus leaking red cells and holding salt and water — not the nephrotic pattern (massive protein, very low albumin, bland urine) his cousin had. Under 13, BP is read against age and height: 128 systolic is past his stage 2 line of 124 (and a diastolic of 84 is not normal even in an adult), so with nephritis it is worked up today. Impetigo four weeks ago fits post-streptococcal GN, which follows a skin infection by 3–6 weeks (a throat infection by 1–3).

Source-supported decision rule; faculty review pending.

• Royal Children's Hospital PSGN clinical practice guideline — Assessment, investigations, treatment, follow-up and nephrology discussion criteria
• AAP pediatric hypertension guideline — Table 3 category definitions and §4.3c ABPM
• AAP Table 4 reproduced by Connecticut Children's — Appendix G, PDF page1: boys age4 and age7, 50th-height column
• AAP 2017 hypertension guideline correction — Correction text
• AAP 2018 hypertension guideline correction — Correction text

Question · Answer and explanation

Objective: aki-01

Creatinine comes from muscle, so a 26-kg child runs far lower than an adult: by the bedside Schwartz equation, a normal GFR at 125 cm corresponds to a creatinine of about 0.4–0.5 — which is what he had. Staged against his own baseline, 0.9 ÷ 0.4 = 2.25, KDIGO 2012 stage 2 (2.0–2.9 times baseline); the acute nephritic illness supports presuming the rise happened this week, but a ten-month-old baseline alone cannot establish that interval. Seek intervening results and follow serial creatinine; document the presumption rather than presenting the clock as proven. Until the creatinine stops moving, every printed or calculated eGFR is invalid.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2012 AKI guideline (current final guideline; 2026 draft not final) — §2.1.1–2/Table2; §2.3.4; §3.8.1–4; §5.1.1–2

Question · Answer and explanation

Objective: glom-13, aki-24

Post-streptococcal GN usually has a favorable course in children, so treatment supports him while the immune complexes clear: salt and fluid limits and a loop diuretic remove the retained volume that drives both the edema and the BP, and the diuretic also helps the kidney excrete potassium. A potassium of 5.3 with a normal ECG needs no calcium — avoid potassium supplements and potassium-containing IV fluids, individualize dietary restriction, and repeat potassium promptly according to its trend and clinical status. Penicillin for 10 days clears any remaining streptococci; it does not treat the nephritis.

Source-supported decision rule; faculty review pending.

• Royal Children's Hospital PSGN clinical practice guideline — Assessment, investigations, treatment, follow-up and nephrology discussion criteria
• CDC Clinical Guidance for PSGN — Diagnosis, Treatment and Prognosis

Question · Answer and explanation

Objective: glom-23, aki-24

The dangerous turns of post-streptococcal GN are hypertensive encephalopathy (headache, vomiting, confusion or a seizure), a falling urine output with a rising creatinine (a nephritis that is not settling, or a rare rapidly progressive course), and fluid in the lungs — each means a same-day visit and a call to pediatric nephrology. The rest is expected recovery: the cola color fades first, microscopic blood can linger for months, protein usually clears within 3–6 months, and streptococcal antibodies can remain elevated after the infection.

Source-supported decision rule; faculty review pending.

• Royal Children's Hospital PSGN clinical practice guideline — Assessment, investigations, treatment, follow-up and nephrology discussion criteria

Question · Answer and explanation

Objective: glom-13, glom-17

Persistent low C3 at ten weeks is atypical enough to reconsider an uncomplicated postinfectious course and arrange pediatric nephrology review now. C3 often normalizes within roughly 6–8 weeks, but no single date proves C3 glomerulopathy. Repeat complement, proteinuria and kidney-function assessment and let the full trajectory guide biopsy.

Clinical application or calculation based on the cited principles; faculty review pending.

• Royal Children's Hospital PSGN clinical practice guideline — Assessment, investigations, treatment, follow-up and nephrology discussion criteria

Question · Answer and explanation

Objective: htn-cardiorenal-17

From 13 on, the AAP 2017 guideline stages blood pressure with the adult cut-points rather than the percentile tables: elevated 120–129/<80, stage 1 130–139/80–89, stage 2 140/90 or higher. His 134 is in the stage 1 office-BP category. Persistent stage 1 readings on three visits call for ambulatory BP monitoring to confirm hypertension; height does not change the adolescent category.

Source-supported decision rule; faculty review pending.

• AAP pediatric hypertension guideline — Table 3 category definitions and §4.3c ABPM
• AAP 2018 hypertension guideline correction — Correction text

Question · Answer and explanation

Objective: glom-01

Chlorhexidine contamination can produce an analytical false-positive protein reaction. The pad mainly detects albumin concentration, so dilute urine or non-albumin proteins can instead yield a falsely reassuring result. Exercise can cause genuine transient proteinuria and concentrated urine can increase the measured protein concentration; neither should be confused with a proven analytical false positive. Confirm an unexpected result with a clean specimen and quantitative protein-to-creatinine or albumin-to-creatinine ratio.

Source-supported decision rule; faculty review pending.

• Siemens urinalysis test-strip instructions — Protein test characteristics and Helpful Hints, PDF pp1–2
• Siemens 2022 urinalysis field safety notice POC22-018.A.OUS — Table2 Protein row, PDF page2

Question · Answer and explanation

Objective: glom-05

One daytime dipstick after exercise cannot separate three different things: transient proteinuria (exercise, fever, stress — gone within a day or two), orthostatic proteinuria (protein made only when upright, common in tall, thin young men and benign), and persistent proteinuria from kidney disease. A first-morning specimen — urine made lying down, overnight, at rest — is the key: if its protein-to-creatinine ratio is normal, the daytime protein was postural or transient, and a daytime sample on a rest day tells which. The trace blood is a separate question that only a microscope answers.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — Tables 1–3 (S137); §4.2 PP4.2.5; §4.3 PP4.3.1–4.3.3; Figure 47; §1.3.1/PP1.3.1.4, S192–193 (first-morning urine and orthostatic proteinuria)
• KDIGO 2021 Glomerular Diseases guideline with 2024 lupus update — PP1.3.1 urine sediment; PP1.4.1–1.4.5 edema; PP3.1.1–3.1.2 membranous diagnosis and associated-cause evaluation

Question · Answer and explanation

Objective: glom-05, glom-03

Protein that appears upright and vanishes overnight is orthostatic proteinuria — generally benign, with periodic blood pressure and urine follow-up. The blood is a separate finding: his 8–10 RBC/hpf exceed the supplied laboratory reference range, and dysmorphic red cells with acanthocytes strongly support a glomerular source. One specimen is not a pattern, and exercise can cause transient hematuria — so repeat microscopy on two more fresh specimens, and ask who else in the family has blood in the urine.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2021 Glomerular Diseases guideline with 2024 lupus update — PP1.3.1 urine sediment; PP1.4.1–1.4.5 edema; PP3.1.1–3.1.2 membranous diagnosis and associated-cause evaluation
• ERKNet/ERA/ESPN Alport guideline 2024 — Diagnosis/genotype discussion; Question17 recommendations17.1–17.4

Question · Answer and explanation

Objective: glom-26, structural-11

The circumstances to notice are which side of the family the disease sits on and that Ethan is a boy. Glomerular hematuria on three samples, a mother with lifelong hematuria and her brother deaf at 30 and on dialysis is the X-linked pattern of type IV collagen disease: heterozygous women may have hematuria and can also develop proteinuria or CKD, while males with X-linked Alport syndrome have kidney involvement in essentially every case, and it progresses. The protein was orthostatic and stays benign, but "reassure and close the chart" is now much less likely; audiometry, an eye exam and genetics come next.

Clinical application or calculation based on the cited principles; faculty review pending.

• ERKNet/ERA/ESPN Alport guideline 2024 — Diagnosis/genotype discussion; Question17 recommendations17.1–17.4

Question · Answer and explanation

Objective: glom-06

Read the cells before the family history: uniform red cells, no protein, no casts and clots strongly suggest a urologic source. Age, sex, smoking history and the degree of bleeding — here visible, with clots — are what the AUA/SUFU risk scheme weighs, and they send him for CT urography (upper tract) and cystoscopy (bladder). Anticoagulation can contribute to bleeding, but does not remove the need to investigate an underlying lesion, and a "UTI" with a negative culture was never proven — hematuria blamed on either must be shown to resolve.

Source-supported decision rule; faculty review pending.

• AUA Medical Student Curriculum: Hematuria — Gross hematuria evaluation section p5
• AUA/SUFU Microhematuria guideline 2025 — Statements4,6 and7

Question · Answer and explanation

Objective: structural-11

Autosomal dominant tubulointerstitial kidney disease can cause progressive CKD with a bland urine sediment. Early gout supports an UMOD-associated form but is not diagnostic. Recognize the family pattern and refer for appropriate genetic evaluation and counseling; a bland urinalysis does not exclude inherited kidney disease.

Source-supported decision rule; faculty review pending.

• KDIGO ADTKD consensus report 2015 — Table2 and UMOD discussion pp3–4

Question · Answer and explanation

Objective: aki-12, aki-06

Drug-induced AIN is an immune-mediated interstitial injury with variable timing and presentation. Sterile pyuria and white-cell casts support it, but are neither required nor specific; the classic fever–rash–eosinophilia triad is often absent. Urine eosinophils neither confirm nor exclude AIN.

Source-supported decision rule; faculty review pending.

• Moledina et al. Urine TNF-alpha and IL-9 for clinical diagnosis of AIN — Introduction; Abstract methods/results; Discussion of clinical diagnostic limitations

Question · Answer and explanation

Objective: structural-23

ACR Category I permits continuation for IV iodinated contrast when there is no AKI and eGFR is at least 30. ACR Category II requires interruption for AKI or eGFR below 30, with reassessment before restart after 48 hours. Metformin itself is not nephrotoxic; accumulation during illness or kidney failure can contribute to lactic acidosis.

Source-supported decision rule; faculty review pending.

• ACR Manual on Contrast Media 2026 — Metformin pp48–49 Category I/II; CA-AKI pp43–44; NSF pp80–82
• Metformin prescribing information — §2.3 renal impairment and §2.4 iodinated contrast

Question · Answer and explanation

Objective: aki-09, structural-21, aki-06

Muddy brown casts and tubular cells favor acute tubular injury after stacked nephrotoxic exposures. The high vancomycin level can contribute to injury and also result from reduced clearance. Hold the next dose and obtain pharmacy/ID review of levels, kidney trend and culture-directed treatment. Current vancomycin guidance favors AUC-guided monitoring; students need to recognize toxicity and request that review, not calculate an AUC.

Clinical application or calculation based on the cited principles; faculty review pending.

• ASHP/IDSA/PIDS/SIDP vancomycin monitoring consensus 2020 — Executive summary
• KDIGO 2012 AKI guideline (current final guideline; 2026 draft not final) — §2.1.1–2/Table2; §2.3.4; §3.8.1–4; §5.1.1–2

Question · Answer and explanation

Objective: aki-12, aki-06

The new inflammatory findings raise concern for superimposed drug-induced AIN, so ATN as the sole explanation becomes less likely. A or B is defensible with that reasoning; the day-6 evidence can still support tubular injury. Neither the rash nor sediment proves two biopsy-defined lesions. Stop the unnecessary beta-lactam, review all possible culprits including vancomycin, and involve nephrology if recovery is delayed.

Clinical application or calculation based on the cited principles; faculty review pending.

• Moledina et al. Urine TNF-alpha and IL-9 for clinical diagnosis of AIN — Introduction; Abstract methods/results; Discussion of clinical diagnostic limitations

Question · Answer and explanation

Objective: aki-10, structural-15, structural-23

Because the limb assessment permits delay, defer and reassess the diagnostic benefit against the evolving AKI. If IV contrast remains needed, use a dose sufficient for diagnosis and isotonic saline prophylaxis when appropriate for his volume status. Hold metformin during AKI and follow restart criteria. Urgent imaging can proceed when the expected benefit outweighs risk.

Source-supported decision rule; faculty review pending.

• ACR Manual on Contrast Media 2026 — Metformin pp48–49 Category I/II; CA-AKI pp43–44; NSF pp80–82
• Metformin prescribing information — §2.3 renal impairment and §2.4 iodinated contrast

Question · Answer and explanation

Objective: aki-25, aki-02

Neither creatinine estimate is reliable during changing kidney function. Review each medicine with pharmacy using its label, toxicity risk, current trend and drug levels where available; do not apply a universal lowest-estimate rule. This patient needs reduced gabapentin and renal-adjusted prophylaxis, with reassessment as function changes; metformin remains held.

Source-supported decision rule; faculty review pending.

• KDIGO 2024 CKD guideline — Tables 1–3 (S137); §4.2 PP4.2.5; §4.3 PP4.3.1–4.3.3; Figure 47; §1.3.1/PP1.3.1.4, S192–193 (first-morning urine and orthostatic proteinuria)
• NEURONTIN prescribing information — §2.3 Table 1 and Cockcroft–Gault equation; §2.5
• LOVENOX current prescribing information — §2.3 Table1 and §2.6

Question · Answer and explanation

Objective: aki-26

Document the AKI stage, incomplete recovery, probable tubular injury and suspected AIN, naming the suspected culprit and reaction rather than asserting a biopsy-proven or blanket class allergy. Arrange early labs during antibiotic treatment and a three-month recovery/CKD review. Restart held medicines only after individualized reassessment; metformin requires stable function and an eligible eGFR.

Source-supported decision rule; faculty review pending.

• KDIGO 2012 AKI guideline (current final guideline; 2026 draft not final) — §2.1.1–2/Table2; §2.3.4; §3.8.1–4; §5.1.1–2
• KDIGO 2024 CKD guideline — Tables 1–3 (S137); §4.2 PP4.2.5; §4.3 PP4.3.1–4.3.3; Figure 47; §1.3.1/PP1.3.1.4, S192–193 (first-morning urine and orthostatic proteinuria)
• Metformin prescribing information — §2.3 renal impairment and §2.4 iodinated contrast

Question · Answer and explanation

Objective: structural-21, aki-09

Aminoglycosides can injure the kidney and inner ear. Reassess whether the drug is necessary, avoid unnecessary nephrotoxic combinations, and have pharmacy individualize dosing and monitoring. Extended intervals do not eliminate toxicity and are not automatically appropriate during unstable AKI.

Source-supported decision rule; faculty review pending.

• KDIGO 2012 AKI guideline (current final guideline; 2026 draft not final) — §2.1.1–2/Table2; §2.3.4; §3.8.1–4; §5.1.1–2
• Gentamicin prescribing information — Boxed Warning, Clinical Pharmacology and Precautions

Question · Answer and explanation

Objective: aki-21

A dying cancer cell empties itself: potassium and phosphate pour out, and its nucleic acids are broken down to uric acid. Phosphate binds calcium, so calcium falls, and uric acid and calcium phosphate crystallize in the tubules, so the creatinine rises. For bedside recognition, look for at least two absolute abnormalities: uric acid ≥8 mg/dL, potassium ≥6.0 mEq/L, phosphorus ≥4.5 mg/dL or corrected calcium ≤7.0 mg/dL around treatment. The original Cairo–Bishop definition also includes relative changes and defines clinical renal involvement as creatinine ≥1.5 times the upper limit of normal; do not confuse that grading rule with KDIGO AKI staging.

Source-supported decision rule; faculty review pending.

• eviQ Prevention of tumour lysis syndrome — Definitions/Cairo–Bishop, risk assessment, hydration, urine alkalinization, allopurinol and rasburicase

Question · Answer and explanation

Objective: lytes-13

Three jobs, three kinds of drug. Stabilize: IV calcium steadies the heart-muscle membrane for 30–60 minutes without lowering potassium at all. Shift: insulin with dextrose — with glucose checks, because hypoglycemia comes late when the kidney is injured — and high-dose nebulized albuterol move potassium into cells for a few hours. Remove: only urine, a gut binder or dialysis takes potassium out of the body; everything else wears off.

Source-supported decision rule; faculty review pending.

• UK Kidney Association Hyperkalemia guideline updated July2026 — Guidelines14.2,16.2a–b,16.3.1–3,16.4.1–3,16.5,16.6 and17.1

Question · Answer and explanation

Objective: aki-21

Russ was high risk on the counts the TLS lecture and handout list — high-grade lymphoma over 10 cm, LDH more than twice normal, uric acid above 7.5, a rising creatinine, a dry patient — and his morning panel already met two Cairo-Bishop criteria. High risk means rasburicase, an enzyme that converts existing uric acid to soluble allantoin (check G6PD first: it causes hemolysis in G6PD deficiency), IV isotonic fluid before chemotherapy, titrated to urine output, and chemistry every 4–6 hours. Allopurinol only blocks new uric acid and takes a day or two to act.

Source-supported decision rule; faculty review pending.

• eviQ Prevention of tumour lysis syndrome — Definitions/Cairo–Bishop, risk assessment, hydration, urine alkalinization, allopurinol and rasburicase
• MD Anderson TLS in adult patients, version7, approved2025-12-16 — Algorithm p1, AppendixA risk p2, AppendixB rasburicase p3, AppendixC electrolytes pp4–5

Question · Answer and explanation

Objective: lytes-13, lytes-17

Hyperkalemia kills first in TLS, and peaked T waves mean the heart is already affected, so IV calcium goes in now — carpal spasm with a long QT is a second, independent reason. Give monitored calcium and reassess the ECG and symptoms; then shift potassium with insulin/dextrose and nebulized albuterol, following serial glucose monitoring. Persistent severe symptoms may require additional specialist-directed calcium. What you do not do is infuse calcium to normalize the number: every milligram meets a phosphorus of 8.9 and can precipitate as calcium phosphate in the kidney. Lower the phosphate, and the calcium follows.

Source-supported decision rule; faculty review pending.

• UK Kidney Association Hyperkalemia guideline updated July2026 — Guidelines14.2,16.2a–b,16.3.1–3,16.4.1–3,16.5,16.6 and17.1
• MD Anderson TLS in adult patients, version7, approved2025-12-16 — Algorithm p1, AppendixA risk p2, AppendixB rasburicase p3, AppendixC electrolytes pp4–5

Question · Answer and explanation

Objective: aki-21, lytes-19, aki-23

Crystals form where urine is scant and concentrated, so the first treatment is flow: potassium-free isotonic saline, a bolus and then a rate individualized to perfusion, hourly urine output and frequent lung/weight reassessment — a kidney full of crystals may not answer. Rasburicase clears the uric acid already there (send later levels on ice, or the enzyme keeps working in the tube); a phosphate binder is an adjunct. No bicarbonate: alkaline urine precipitates calcium phosphate, and urinary alkalinization is no longer recommended in TLS.

Source-supported decision rule; faculty review pending.

• eviQ Prevention of tumour lysis syndrome — Definitions/Cairo–Bishop, risk assessment, hydration, urine alkalinization, allopurinol and rasburicase
• MD Anderson TLS in adult patients, version7, approved2025-12-16 — Algorithm p1, AppendixA risk p2, AppendixB rasburicase p3, AppendixC electrolytes pp4–5

Question · Answer and explanation

Objective: aki-21

The chemistry already strongly establishes TLS. Needle-like crystals raise concern for an additional crystal nephropathy in a dehydrated patient receiving IV acyclovir, but morphology alone does not identify the material: uric acid can also form needles. Retain TLS and investigate a possible concurrent drug-related injury. Review acyclovir indication, renal dosing, infusion rate and hydration with pharmacy; do not turn a suggestive sediment finding into a proven second diagnosis.

Clinical application or calculation based on the cited principles; faculty review pending.

• eviQ Prevention of tumour lysis syndrome — Definitions/Cairo–Bishop, risk assessment, hydration, urine alkalinization, allopurinol and rasburicase
• Acyclovir injection prescribing information — Warnings, Precautions and Dosage renal Table5

Question · Answer and explanation

Objective: aki-16, aki-25

Rapid IV acyclovir in a dehydrated patient with impaired clearance increases crystal-injury risk. The label requires infusion over at least one hour, adequate hydration and renal adjustment. The crystals suggest a possible additional process, not chemical proof; urgently balance antiviral need against toxicity and adjust the next order.

Source-supported decision rule; faculty review pending.

• Acyclovir injection prescribing information — Warnings, Precautions and Dosage renal Table5

Question · Answer and explanation

Objective: aki-22, aki-24, lytes-19

Dialysis treats complications, not numbers, and Russ now has three: hyperkalemia back with ECG changes despite treatment, phosphate climbing with symptomatic hypocalcemia, and oliguria with fluid in his lungs — the E and O of AEIOU plus TLS's own phosphate trigger. Calcium again for the ECG and the spasm, no more saline, and call now, because dialysis takes time to arrange. Know its limits: it removes potassium, phosphate, uric acid and fluid, but the lymphoma keeps dying, so levels rebound after each session — recheck every few hours and expect more than one session.

Source-supported decision rule; faculty review pending.

• KDIGO 2012 AKI guideline (current final guideline; 2026 draft not final) — §2.1.1–2/Table2; §2.3.4; §3.8.1–4; §5.1.1–2
• UK Kidney Association Hyperkalemia guideline updated July2026 — Guidelines14.2,16.2a–b,16.3.1–3,16.4.1–3,16.5,16.6 and17.1
• MD Anderson TLS in adult patients, version7, approved2025-12-16 — Algorithm p1, AppendixA risk p2, AppendixB rasburicase p3, AppendixC electrolytes pp4–5

Question · Answer and explanation

Objective: aki-20, lytes-07

Splanchnic vasodilation lowers effective arterial filling despite excess total-body water. Neurohormonal activation promotes sodium retention, impaired water excretion and renal vasoconstriction. This mechanism explains the pattern, but does not diagnose HRS or prove fluid responsiveness.

Source-supported decision rule; faculty review pending.

• ADQI–ICA AKI in cirrhosis consensus2024 — HRS-AKI criteria; volume assessment/resuscitation and fluid choice; HRS management recommendations

Question · Answer and explanation

Objective: aki-05

FENa is most informative in the selected oliguric patient with no CKD and no recent diuretic exposure, interpreted with the examination and sediment. A low value supports sodium avidity, while a high value may support impaired sodium reabsorption; neither proves a mechanism. Diuretic exposure, CKD, sepsis and cirrhosis reduce its diagnostic discrimination. The test cannot replace reassessment of the patient or determine fluid responsiveness by itself.

Clinical application or calculation based on the cited principles; faculty review pending.

• Espinel and Gregory, Differential diagnosis of acute renal failure1980 — Abstract
• ADQI–ICA AKI in cirrhosis consensus2024 — HRS-AKI criteria; volume assessment/resuscitation and fluid choice; HRS management recommendations

Question · Answer and explanation

Objective: aki-20, structural-20, aki-23

He appears intravascularly depleted despite ascites. Stop contributing drugs, obtain prompt diagnostic paracentesis, assess obstruction and restore volume with small reassessed amounts of balanced crystalloid. Albumin has specific indications, including SBP with AKI, rather than being mandatory for every cirrhotic AKI. A low FENa does not separate these phenotypes.

Source-supported decision rule; faculty review pending.

• ADQI–ICA AKI in cirrhosis consensus2024 — HRS-AKI criteria; volume assessment/resuscitation and fluid choice; HRS management recommendations
• AASLD ascites/SBP practice guidance 2021 — SBP and other spontaneous infections; Management of SBP; Guidance statements
• AASLD Why Timing Matters: Paracentesis on Admission for Cirrhosis with Ascites — Interpreting PMN count and culture

Question · Answer and explanation

Objective: lytes-07

He has cirrhotic water retention with a superimposed volume-depletion component. Restore lost perfusion first, then reassess water restriction and ongoing fluid need. A fixed saline infusion until sodium reaches 135 ignores volume status and risks overcorrection; advanced liver disease increases osmotic-demyelination risk, so target a modest rise with a maximum of 8 mEq/L in 24 hours.

Source-supported decision rule; faculty review pending.

• ADQI–ICA AKI in cirrhosis consensus2024 — HRS-AKI criteria; volume assessment/resuscitation and fluid choice; HRS management recommendations
• UK Kidney Association Hyperkalemia guideline updated July2026 — Guidelines14.2,16.2a–b,16.3.1–3,16.4.1–3,16.5,16.6 and17.1
• AASLD ascites/SBP practice guidance 2021 — SBP and other spontaneous infections; Management of SBP; Guidance statements
• AASLD Why Timing Matters: Paracentesis on Admission for Cirrhosis with Ascites — Interpreting PMN count and culture

Question · Answer and explanation

Objective: aki-04

Failure to improve after adequate resuscitation makes a solely volume-responsive explanation much less likely. HRS-AKI becomes a leading consideration, but normal-looking sediment does not exclude tubular injury and drug injury can persist after exposure stops. Continue the differential while promptly reassessing for HRS treatment.

Clinical application or calculation based on the cited principles; faculty review pending.

• ADQI–ICA AKI in cirrhosis consensus2024 — HRS-AKI criteria; volume assessment/resuscitation and fluid choice; HRS management recommendations

Question · Answer and explanation

Objective: aki-20, htn-cardiorenal-26

Established HRS-AKI is treated with a vasoconstrictor given with albumin, which narrows the dilated gut vessels so blood returns to the arteries and the kidneys. Choosing the drug (terlipressin, or norepinephrine when terlipressin cannot be used), dosing it and watching for its serious harms — breathing failure and ischemia — belong to the specialists; your move is to recognize it and call today. A liver transplant treats the circulation that caused this, and transplant evaluation should be expedited using an individualized candidacy assessment, not a fixed sobriety-period rule.

Source-supported decision rule; faculty review pending.

• ADQI–ICA AKI in cirrhosis consensus2024 — HRS-AKI criteria; volume assessment/resuscitation and fluid choice; HRS management recommendations

Question · Answer and explanation

Objective: structural-06, structural-25

Frequency, urgency and nocturia are storage symptoms an obstructed outlet produces by itself: a bladder that never empties is always nearly full, so it signals often and spills small amounts (overflow). Anticholinergics — oxybutynin, and the diphenhydramine in "PM" sleep aids — relax the bladder muscle and can turn partial retention into complete retention. A bladder scan after he voids settles it in a minute; interpret the residual with symptoms and repeated measurements; no single cutoff defines all clinically important retention.

Source-supported decision rule; faculty review pending.

• AUA Urologic Emergencies medical-student guidance — Acute urinary retention and postobstructive diuresis sections
• AUA BPH guideline amendment2023 — Statements23–25 acute retention and trial without catheter

Question · Answer and explanation

Objective: lytes-23

The serum gap is 138 − (114 + 16) = 8; the urine gap is (30 + 25) − 75 = −20. In this simplified normal-gap acidosis, a negative urine gap supports ammonium excretion and an extrarenal bicarbonate loss such as diarrhea. It is an indirect clue, not an ammonium measurement; ketonuria, other urinary anions and very low urine sodium can invalidate the shortcut.

Source-supported decision rule; faculty review pending.

• Batlle et al. Urinary anion gap in hyperchloremic metabolic acidosis1988 — Abstract

Question · Answer and explanation

Objective: aki-17, structural-06

Painful high-volume retention needs prompt drainage and withdrawal of aggravating anticholinergics. It strongly suggests a postrenal contribution, which the subsequent ultrasound and improvement support; the bladder scan alone does not prove that obstruction is the only AKI cause. Recheck potassium and kidney function and monitor urine output after drainage.

Source-supported decision rule; faculty review pending.

• AUA Urologic Emergencies medical-student guidance — Acute urinary retention and postobstructive diuresis sections
• KDIGO 2012 AKI guideline (current final guideline; 2026 draft not final) — §2.1.1–2/Table2; §2.3.4; §3.8.1–4; §5.1.1–2

Question · Answer and explanation

Objective: lytes-14, lytes-23, lytes-24

Obstruction can impair distal potassium and acid excretion, producing a type-4-like hyperkalemic normal-gap acidosis. The positive urine gap supports this interpretation in context, but does not directly prove low ammonium, particularly in changing kidney function. Drain the obstruction and reassess the biochemical response.

Clinical application or calculation based on the cited principles; faculty review pending.

• Batlle et al. Urinary anion gap in hyperchloremic metabolic acidosis1988 — Abstract
• UK Kidney Association Hyperkalemia guideline updated July2026 — Guidelines14.2,16.2a–b,16.3.1–3,16.4.1–3,16.5,16.6 and17.1
• AUA Urologic Emergencies medical-student guidance — Acute urinary retention and postobstructive diuresis sections

Question · Answer and explanation

Objective: aki-18, structural-08

Sustained output above 200 mL/h after relief of obstruction calls for monitoring for volume and electrolyte losses. Because he cannot drink reliably, give individualized replacement guided by examination, sodium and losses; a partial replacement fraction is a starting approach, not a universal formula. Fluid composition and frequency of labs must follow the trajectory.

Clinical application or calculation based on the cited principles; faculty review pending.

• AUA Urologic Emergencies medical-student guidance — Acute urinary retention and postobstructive diuresis sections

Question · Answer and explanation

Objective: structural-04

A positive culture sounds like confirmation; that is the trap. Bacteriuria is common with impaired emptying, and without localizing symptoms or systemic signs that is asymptomatic bacteriuria, which IDSA 2019 advises not to treat; the pyuria travels with it. Urosepsis needs a body responding to infection — for 48 hours there was none — and the confusion and belly ache had a better explanation that resolved without antibiotics. New fever, flank pain or rigors require prompt reassessment for symptomatic infection. A planned endourologic procedure expected to cause mucosal trauma is a separate indication for culture-directed peri-procedural treatment.

Clinical application or calculation based on the cited principles; faculty review pending.

• IDSA Asymptomatic Bacteriuria guideline2019 — SectionV older adults with delirium; SectionXIII endourologic procedures

Question · Answer and explanation

Objective: structural-06, structural-25

Restarting at 0.4 mg approximately 30 minutes after the same meal follows the tamsulosin label. Prior dizziness still matters even if today’s drop misses the orthostatic threshold: discuss falls, reassess standing symptoms and other BP medicines. AUA advises at least three days of alpha-blocker treatment before a trial without catheter; the enlarged gland and renal complication warrant urology review for additional medical or procedural treatment.

Source-supported decision rule; faculty review pending.

• AUA BPH guideline amendment2023 — Statements23–25 acute retention and trial without catheter
• Tamsulosin prescribing information — §2 dose administration and §5.1 orthostasis
• ELIQUIS prescribing information — §2.1 and §8.6 NVAF dosing

Question · Answer and explanation

Objective: glom-19

Nephrotic syndrome increases thrombosis risk. The acute pain, hematuria and kidney-function change warrant urgent vascular evaluation while other causes of AKI are assessed. An empty bladder excludes neither ureteral obstruction nor vascular disease.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2021 membranous nephropathy — p1, takeaway 5 and Figure 2: thrombosis risk; acute symptom interpretation is a clinical inference

Question · Answer and explanation

Objective: aki-20, aki-05, htn-cardiorenal-26

Sodium avidity is common in cirrhosis and is not a fluid-response test. Persistent AKI after appropriate resuscitation raises concern for hepatorenal physiology, but the assessment remains clinical and may involve more than one mechanism. Obtain hepatology/nephrology input; routine prolonged albumin administration without assessing volume can cause harm.

Clinical application or calculation based on the cited principles; faculty review pending.

• ADQI–ICA joint consensus on AKI in cirrhosis (2024) — Diagnostic criteria for HRS-AKI, Box 1; fluid assessment and FENa limitations

Question · Answer and explanation

Objective: lytes-03, lytes-21, aki-01

Read Na → K → Cl → bicarbonate → anion gap → BUN/creatinine → glucose, then Ca/Mg/phosphorus. AG = 128 − (96 + 14) = 18; albumin is normal. Creatinine is three times a recent baseline. Obtain an ECG and urgently manage confirmed hyperkalemia according to the clinical protocol while evaluating AKI and the acid-base disorder; a blood gas and cause-directed tests complete the assessment.

Clinical application or calculation based on the cited principles; faculty review pending.

• KDIGO 2012 AKI guideline — 2.1.1–2.1.2 and Table 2: recent-baseline AKI criteria and staging
• UKKA hyperkalemia guideline, July 2026 — 14.1–14.2 and hospital management recommendations: urgent ECG assessment and treatment

Question · Answer and explanation