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Question and answer links
- Q1: A 71-year-old woman with a serum albumin of 2.4 g/dL has a total calcium of 11.2 mg/dL. What is her albumin-corrected ca · Answer
- Q2: A patient has a confirmed, albumin-corrected calcium of 12.8 mg/dL. Which single test organizes the entire differential · Answer
- Q3: A 67-year-old man with type 2 diabetes takes metformin 1,000 mg twice daily. His steady-state eGFR, which was 58 mL/min/ · Answer
- Q4: Corrected calcium 14.4 mg/dL, new confusion, creatinine 2.3 mg/dL (baseline 1.0), sodium 149 mEq/L, orthostatic. What is · Answer
- Q5: Creatinine 2.3 from 1.0, BUN 52, orthostatic and dry, ultrasound without hydronephrosis, a post-void residual of 40 mL, · Answer
- Q6: Corrected calcium 14.4 mg/dL with an intact PTH of 8 pg/mL. He takes a thiazide, chews 8–10 calcium-carbonate tablets a · Answer
- Q7: Hour 1 in the ED: the first liter of isotonic saline is in and the second is running at 250 mL/hour. He is still confuse · Answer
- Q8: Two months ago: painless gross hematuria for two days in a 67-year-old smoker, >100 RBC/hpf with normal (isomorphic) red · Answer
- Q9: If you were thinking "his hypercalcemia is milk-alkali syndrome from the calcium carbonate, with the thiazide adding to · Answer
- Q10: Day 2: creatinine 1.6 mg/dL and falling (baseline 1.0), so still in active AKI. The 5.1-cm solid vascular left renal mas · Answer
- Q11: Day 6, going home: creatinine 1.3 mg/dL (1.0 six months ago, 2.3 on arrival), metformin held, the thiazide stopped, the · Answer
- Q12: A 63-year-old patient has intermittent painless visible hematuria and 4 kg of unexplained weight loss. Renal-protocol CT · Answer
Session S4 · 2026-10-29 · in-session · 37 min Anchor: Acute kidney injury — AKI with a hypercalcemia differential and an incidental solid renal mass · Integrates: PTH-dependent vs PTH-independent hypercalcemia, nephrogenic DI, simple vs complex cyst, RCC red flags, imaging and contrast with an injured kidney, hematuria routing, creatinine-bump triage, post-AKI follow-up, urology / oncology referral One-line hook: The ultrasound you ordered for the creatinine shows a mass. The calcium still has to be explained step by step before anyone names a cause.
Learning Objectives
Answers for this section: Q1 · Q2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12
- Decide where and how fast an outpatient with a creatinine bump, an albumin-corrected calcium of 14.4 mg/dL and new confusion is evaluated, and explain the reasoning.
- Sort a hypercalcemia-driven AKI into the prerenal / intrinsic / post-renal frame using the BMP, the urinalysis with microscopy, and a renal and bladder ultrasound.
- Correct a total calcium for albumin, order intact PTH first, and run the PTH-independent walk (PTHrP, vitamin D metabolites, SPEP/UPEP and free light chains, milk-alkali, thiazide, immobilization) before naming the cause.
- Give the emergency treatment sequence adjusted for an injured kidney — isotonic saline with reassessment, calcitonin for speed and prompt renal-informed antiresorptive treatment with the specialist, stop excess calcium and the thiazide, hold vitamin D during the acute evaluation and hold metformin — and say why the loop diuretic waits.
- Separate a simple cyst from a solid mass, choose imaging for an enhancing mass when the kidney is injured, route hematuria to urology, and plan the follow-up an AKI needs after discharge (RCC red flags and referral are tested in the required post-session Q12).
Warm-Up (individual commit before the case)
Answers for this section: Q1 · Q2 · Q3
Three readiness items. Cards up on each; no team discussion yet.
Q1Correct the calcium
A 71-year-old woman with a serum albumin of 2.4 g/dL has a total calcium of 11.2 mg/dL. What is her albumin-corrected calcium?
10.5 mg/dL
11.2 mg/dL
12.5 mg/dL
13.8 mg/dL
Show answer and explanation · Link to this question
Correct answer: C
Learning point: 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. Why not the others: A corrects in the wrong direction; B skips the correction; D adds about twice the correction. Course reading: Evidence for this case
Q2The first test
A patient has a confirmed, albumin-corrected calcium of 12.8 mg/dL. Which single test organizes the entire differential and should be sent first?
Parathyroid hormone-related protein (PTHrP)
Intact parathyroid hormone (PTH)
25-hydroxyvitamin D
Serum protein electrophoresis (SPEP)
Show answer and explanation · Link to this question
Correct answer: B
Learning point: 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. Why not the others: A, C and D are second-step tests on the PTH-suppressed branch; ordered first, they cannot tell you whether the parathyroids are driving or following. Course reading: Evidence for this case
Q3Metformin and a falling eGFR
A 67-year-old man with type 2 diabetes takes metformin 1,000 mg twice daily. His steady-state eGFR, which was 58 mL/min/1.73 m² last year, is now 27 mL/min/1.73 m². What do you do with the metformin?
Continue 1,000 mg twice daily and recheck the eGFR in 3 months
Reduce the dose to 500 mg twice daily and recheck in 3 months
Continue it, and stop only if a lactate level comes back elevated
Stop the metformin now and adjust the rest of his diabetes plan
Show answer and explanation · Link to this question
Correct answer: D
Learning point: 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. Why not the others: A ignores the stop threshold; B is the right move one band higher (eGFR 30–45), not at 27; C waits for the complication you are trying to prevent. Course reading: Evidence for this case
Part 1 — Presentation
Answers for this section: Q4 · Q5 · Q6
Mr. Russell Keane is a 67-year-old retired machinist who comes to your clinic in Dubuque because his daughter is worried. For about three weeks he has been "not himself" — misplacing things, repeating questions, dozing in the afternoon. He is up four or five times a night to urinate and drinks a pitcher of water a day. He has been constipated for a month despite a stool softener, and his appetite is poor. The clinic scale reads 74 kg; six months ago it read 80 kg.
He has smoked a pack a day since he was nineteen — 48 pack-years — and still does. He has type 2 diabetes for 11 years (last HbA1c 7.4%), hypertension, reflux and hyperlipidemia. No prior kidney disease: a creatinine of 1.0 mg/dL six months ago, with a printed eGFR of 82.
When you ask about the reflux he pulls a roll of chewable calcium-carbonate antacids out of his jacket. He chews "eight, maybe ten a day, more after supper," and has for about a year. He also takes an over-the-counter vitamin D3 "for his bones."
One more item, buried in the chart. Two months ago he went to an urgent-care clinic with two days of painless, pink-to-red urine. The urinalysis showed 3+ blood with more than 100 RBC/hpf, and the microscopy comment read "RBCs of normal morphology." No protein, no casts. The culture was negative. He was told it was "probably a bladder irritation," asked to recheck in a week, and the repeat urinalysis was clear. Nobody followed up.
Vitals (clinic, lying then standing): BP 108/66 mmHg lying → 86/54 standing · pulse 98 lying → 118 standing · T 36.9 °C · respirations 16/min · SpO₂ 96% on room air · weight 74 kg (80 kg six months ago).
Exam: Thin, slowed, oriented to person and place but not the date; answers after a pause. Dry mucous membranes, poor skin turgor, flat neck veins at 30 degrees. Lungs with prolonged expiration, no crackles. Heart regular, no murmur. Abdomen soft, mildly distended, no palpable mass, no flank or costovertebral-angle tenderness. No edema. Deep tendon reflexes 1+ and symmetric. No focal neurologic deficit.
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| Hydrochlorothiazide | 25 mg | PO | daily | Hypertension |
| Metformin | 1,000 mg | PO | twice daily | Type 2 diabetes |
| Atorvastatin | 20 mg | PO | nightly | Hyperlipidemia |
| Calcium carbonate chewable (OTC) | 500 mg per tablet (200 mg elemental calcium) | PO | 8–10 tablets daily | Reflux (self-directed) |
| Vitamin D3 (OTC) | 2,000 IU | PO | daily | "Bone health" (self-directed) |
| Docusate | 100 mg | PO | twice daily | Constipation |
You draw a BMP, a calcium and albumin, and a CBC in clinic. The results come back within the hour.
| Test | Result | Reference range |
|---|---|---|
| Sodium | 149 mEq/L | 135–145 |
| Potassium | 3.9 mEq/L | 3.5–5.0 |
| Chloride | 107 mEq/L | 98–107 |
| Bicarbonate | 31 mEq/L | 22–28 |
| BUN | 52 mg/dL | 7–20 |
| Creatinine | 2.3 mg/dL (1.0 six months ago) | 0.7–1.3 |
| eGFR (lab-printed, CKD-EPI 2021) | 30 mL/min/1.73 m² — not valid, creatinine is moving | ≥60 |
| Glucose | 148 mg/dL | 70–99 (fasting) |
| Calcium, total | 13.9 mg/dL | 8.5–10.5 |
| Albumin | 3.4 g/dL | 3.5–5.0 |
| Calcium, albumin-corrected | 14.4 mg/dL — 13.9 + 0.8 × (4.0 − 3.4) | 8.5–10.5 |
| Anion gap | 11 — 149 − (107 + 31) | 8–12 |
| BUN:creatinine | 23:1 — 52 ÷ 2.3 | 10–20:1 |
| Hemoglobin | 12.8 g/dL | 13.5–17.5 |
| WBC | 7.2 × 10³/µL | 4.0–11.0 |
| Platelets | 240 × 10³/µL | 150–400 |
For now: a confused 67-year-old smoker, a corrected calcium of 14.4, a creatinine 2.3 times baseline (a ratio compatible with stage 2 if the rise occurred within 7 days; a six-month-old baseline alone cannot establish AKI timing or stage, and the printed eGFR is unreliable while creatinine changes), a sodium of 149, a mild metabolic alkalosis — and a pocketful of calcium carbonate.
Pause — commit before the reveal
Q4Where does he go today?
Corrected calcium 14.4 mg/dL, new confusion, creatinine 2.3 mg/dL (baseline 1.0), sodium 149 mEq/L, orthostatic. What is the right disposition from clinic?
Stop the thiazide and the antacids today; recheck the BMP and calcium in 48–72 hours
Send him to the emergency department now for IV saline and cardiac monitoring
Order PTH, PTHrP and a renal ultrasound as an outpatient; see him back in one week
Start oral furosemide, tell him to push oral fluids, and recheck his labs tomorrow
Show answer and explanation · Link to this question
Correct answer: B
Learning point: 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. Why not the others: A is the right medication change on the wrong timeline — a 48–72-hour recheck is for a stable, asymptomatic bump; C orders the right tests from the wrong venue; D gives a loop diuretic to a dry man, which deepens the volume loss and the AKI. Course reading: Evidence for this case
He goes to the ED by wheelchair with his daughter. The ED physician agrees, places a monitor, starts isotonic saline, and — because this is an unexplained AKI — orders a renal and bladder ultrasound. It is done within two hours.
Renal and bladder ultrasound (ED, same afternoon): - Right kidney 11.2 cm, normal cortical thickness. A 2.0-cm thin-walled, anechoic cyst at the upper pole with posterior acoustic enhancement; no internal echoes, septa, calcification or wall thickening. - Left kidney 12.0 cm. A 5.1-cm heterogeneous, solid, hypoechoic-to-isoechoic mass at the mid-to-lower pole with internal vascularity on color Doppler. - No hydronephrosis on either side. No stones. - Bladder decompressed; post-void residual 40 mL.
Two findings in one picture: on the right a cyst you can describe in a sentence, on the left a mass with its own blood supply. Hold the mass for Part 3 — it does not change the next six hours, but it has already changed the differential for the calcium.
Q5Sort the AKI
Creatinine 2.3 from 1.0, BUN 52, orthostatic and dry, ultrasound without hydronephrosis, a post-void residual of 40 mL, and an ED dipstick negative for blood and protein. Into which compartment does his kidney injury fall, and by what mechanism?
Intrinsic: acute tubular necrosis caused by the hydrochlorothiazide
Post-renal: the left renal mass is obstructing the collecting system
Intrinsic: a paraneoplastic glomerulonephritis caused by the tumor
Prerenal: calcium-driven water loss and renal vasoconstriction
Show answer and explanation · Link to this question
Correct answer: D
Learning point: 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. Why not the others: A — the exposure and findings do not establish thiazide-induced tubular necrosis. B — the mass is not visibly obstructing the system. C — glomerulonephritis is less supported without proteinuria or an active sediment, but urine testing is not an absolute exclusion test. Course reading: Evidence for this case
The ED sends a stat intact PTH. It is back in three hours.
Intact PTH: 8 pg/mL (reference 15–65). Suppressed.
Q6The walk when PTH is suppressed
Corrected calcium 14.4 mg/dL with an intact PTH of 8 pg/mL. He takes a thiazide, chews 8–10 calcium-carbonate tablets a day, has lost 6 kg, and a solid vascular mass sits in his left kidney. Which set of tests comes next?
PTHrP, 25-OH and 1,25-(OH)₂ vitamin D, SPEP, free light chains, chest film
Neck ultrasound plus a sestamibi scan to localize a parathyroid adenoma
A 24-hour urine calcium and a calcium-to-creatinine clearance ratio
Stop the thiazide and the antacids, then repeat the PTH and calcium in a week
Show answer and explanation · Link to this question
Correct answer: A
Learning point: 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). Why not the others: B and C belong to the PTH-dependent branch (adenoma localization; the urine test for familial hypocalciuric hypercalcemia); D is the move when a thiazide may be unmasking primary hyperparathyroidism with a non-suppressed PTH — his is 8, a calcium this high requires evaluation for additional causes, and a week's wait at this level is unsafe. Course reading: Evidence for this case
Part 2 — Data
Answers for this section: Q7 · Q8 · Q9
The full ED panel, drawn before the first liter finished.
| Test | Result | Reference range |
|---|---|---|
| Phosphorus | 2.3 mg/dL | 2.5–4.5 |
| Magnesium | 1.9 mg/dL | 1.7–2.4 |
| Alkaline phosphatase | 96 U/L | 40–130 |
| Serum osmolality, measured | 324 mOsm/kg | 275–295 |
| Serum osmolality, calculated | 325 mOsm/kg — 2 × 149 + 148/18 + 52/2.8 | — |
| TSH | 1.8 mIU/L | 0.4–4.0 |
| Lactate | 1.4 mmol/L | 0.5–2.0 |
| ECG | Sinus tachycardia 104/min, QTc 340 ms (short), no arrhythmia | QTc 350–450 |
| Chest radiograph | Emphysematous changes; no mass, no nodule, no hilar adenopathy | — |
Urinalysis (ED, clean catch):
| Component | Result | Reference |
|---|---|---|
| Color / clarity | Pale yellow, clear | — |
| Specific gravity | 1.006 | 1.005–1.030 |
| pH | 7.0 | 5.0–8.0 |
| Protein | Negative | Negative |
| Blood | Negative | Negative |
| Glucose | Negative | Negative |
| Leukocyte esterase / nitrite | Negative / negative | Negative |
| Urine osmolality | 165 mOsm/kg | 300–900 (should exceed serum when the patient is dry) |
| Microscopy | 0–2 RBC/hpf, 0–2 WBC/hpf, occasional hyaline casts, no granular casts, no crystals, no bacteria | — |
Two things to notice before the questions.
First, the urine is dilute in a dry man. The rule that prerenal AKI makes a concentrated urine (specific gravity above 1.020) assumes the kidney can concentrate; his cannot. A serum osmolality of 324 with a urine osmolality of 165 is the signature of diabetes insipidus: ADH is high, and the collecting duct cannot answer it because calcium has disabled its water channels — which is why the hypernatremia and the volume depletion travel together. His free-water deficit is modest — total body water about 0.5 × 74 kg = 37 L in an older man, deficit ≈ 37 × (149/140 − 1) ≈ 2.4 L — and most of it corrects by mouth as he wakes and drinks and the calcium falls. Volume comes first, and the sodium is rechecked every 4–6 hours, because a kidney making dilute urine can let the sodium climb even on saline.
Second, do not send a FENa. He took hydrochlorothiazide this morning; a thiazide pushes sodium into the urine and makes the fractional excretion of sodium read "intrinsic" when it is not. The sediment and ultrasound support the initial differential; neither definitively excludes intrinsic injury.
Pause — commit before the reveal
Q7What goes with the saline?
Hour 1 in the ED: the first liter of isotonic saline is in and the second is running at 250 mL/hour. He is still confused and his neck veins are still flat; corrected calcium 14.4 mg/dL, creatinine 2.3 mg/dL. What do you add now?
Furosemide 40 mg IV now, so the saline carries more calcium out in the urine
Calcitonin now, with prompt renal-informed antiresorptive treatment arranged alongside rehydration
Zoledronic acid 4 mg IV now instead of calcitonin, because its effect lasts weeks
Urgent hemodialysis tonight, because his kidneys cannot clear the calcium load
Show answer and explanation · Link to this question
Correct answer: B
Learning point: 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. Why not the others: A gives a loop diuretic to a man who is still dry, deepening the volume loss and the AKI; C mistakes duration for speed and doses a dry, injured kidney before repletion; D is for hypercalcemia that fails treatment in a kidney that cannot respond — he has had one liter. Course reading: Evidence for this case
The admitting team pulls the full urgent-care note from two months ago. It confirms the chart summary and records no imaging and no referral.
Q8The hematuria that was filed away
Two months ago: painless gross hematuria for two days in a 67-year-old smoker, >100 RBC/hpf with normal (isomorphic) red-cell morphology, no protein, no casts, negative culture; the urine cleared within a week. What should that episode have triggered?
Nothing more — the urine cleared in a week and the culture was negative
Nephrology referral for complements, ANCA and anti-GBM antibodies
Urology referral: CT urography once the kidney allows, and cystoscopy
A repeat urinalysis in 6 months, with reassurance in the meantime
Show answer and explanation · Link to this question
Correct answer: C
Learning point: 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. Why not the others: A — a negative culture removes the infection explanation rather than closing the case; B is the route for dysmorphic cells, casts or protein, none of which he had; D is the low-risk pathway, which he was never in. Course reading: Evidence for this case
The next 48 hours. Antiresorptive treatment planning begins on admission, alongside rehydration; the later administration below is this patient's selected course, not a rule to delay all patients until creatinine improves. He receives 1 L of isotonic saline over the first hour, then 250 mL/hour, with neck veins, lungs, weight and urine output checked every few hours and a BMP every 6 hours; he never becomes overloaded, so he never needs furosemide. Urine output climbs to about 150 mL/hour. Calcitonin 300 units subcutaneously every 12 hours begins in the ED. Hydrochlorothiazide, calcium carbonate and vitamin D3 are stopped; metformin is held and basal insulin covers the glucose. By the morning of day 1 he knows the date. On day 2, with the creatinine down to 1.6 (Cockcroft–Gault creatinine clearance about 47 mL/min — only an estimate while the creatinine is still moving), the team selects renal-informed antiresorptive therapy with nephrology and pharmacy and follows creatinine and calcium daily. Calcitonin stops after 48 hours.
| Time | Total Ca (mg/dL) | Corrected Ca (albumin 3.4) | Creatinine (mg/dL) | Na (mEq/L) | HCO₃ (mEq/L) | Status |
|---|---|---|---|---|---|---|
| Day 0, ED | 13.9 | 14.4 | 2.3 | 149 | 31 | Confused, orthostatic |
| Day 1 | 12.8 | 13.3 | 1.9 | 146 | 29 | Oriented × 3, drinking |
| Day 2 | 12.0 | 12.5 | 1.6 | 144 | 27 | Zoledronic acid given |
| Day 4 | 10.8 | 11.3 | 1.4 | 142 | 26 | Ambulating; MRI done |
| Day 5 | 10.1 | 10.6 | 1.3 | 141 | 25 | Urology and oncology consults |
Most of the walk returns on day 2; the PTHrP is a send-out test and is still pending:
| Test | Result | Reference range | Read |
|---|---|---|---|
| Intact PTH | 8 pg/mL | 15–65 | Suppressed — PTH-independent branch |
| PTHrP | Pending (send-out lab) | <2.0 pmol/L | — |
| 25-OH vitamin D | 34 ng/mL | 30–100 | Normal — no vitamin D intoxication |
| 1,25-(OH)₂ vitamin D | 18 pg/mL | 18–72 | Low-normal — appropriately suppressed; not granulomatous |
| SPEP | No monoclonal protein | — | Not myeloma |
| Serum free light chains | κ 14.2 / λ 11.8 mg/L, ratio 1.20 | ratio 0.26–1.65 | Normal |
| UPEP | Negative | — | Normal |
Late on day 2 the PTHrP comes back.
Q9Evidence update
Concordance-style practice: there is no expert panel behind this key, the teaching explanation. "Unchanged" means the finding does not move the hypothesis — not "I'm not sure."
If you were thinking "his hypercalcemia is milk-alkali syndrome from the calcium carbonate, with the thiazide adding to it" — and you then learn that his PTHrP is 6.8 pmol/L (reference <2.0) with an intact PTH of 8 pg/mL — this hypothesis, as the MAIN cause, becomes:
Much less likely
Less likely
Unchanged
More likely
Much more likely
Show answer and explanation · Link to this question
Correct answer: A
Formative evidence update: The letter is a teaching anchor. Accept a justified adjacent response; this is not an expert-panel-validated score. Learning point: 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. Why not the others: B undersells a finding neither benign cause can produce; C fits a finding equally compatible with both stories, which describes the PTH of 8, not the PTHrP; D and E move the wrong way. Course reading: Evidence for this case
Part 3 — Course and Decisions
Answers for this section: Q10 · Q11
The mass. On day 2 the team turns to the left kidney. He has most of the short list of red flags for renal cell carcinoma: painless hematuria (two months ago), weight loss (6 kg), smoking (48 pack-years), a solid vascular mass, and a paraneoplastic syndrome — PTHrP hypercalcemia is a classic one. Flank pain and a palpable mass complete the old triad with hematuria; he has neither, and most kidney cancers found incidentally have none of the triad. Ultrasound has shown a solid lesion with blood flow, but it cannot show enhancement — whether the mass takes up contrast — the feature that separates a tumor from its mimics; that takes a multiphasic CT or MRI, with images before contrast and at timed points after it. Macroscopic fat often favors an angiomyolipoma, but the radiologist must assess the complete pattern rather than treating fat alone as definitive.
Pause — commit before the reveal
Q10Imaging an enhancing mass with an injured kidney
Radiology confirms that MRI can answer the enhancement and staging questions without delaying care. The team wants an adequate study that avoids iodinated contrast during this episode of AKI.
Day 2: creatinine 1.6 mg/dL and falling (baseline 1.0), so still in active AKI. The 5.1-cm solid vascular left renal mass needs characterization and staging. Which imaging do you order?
Multiphasic contrast-enhanced CT of the abdomen now, the standard mass study
Non-contrast CT of the abdomen now, to avoid contrast while the kidney recovers
MRI of the abdomen now with a group II gadolinium-based contrast agent
Repeat renal ultrasound in 3 months to see whether the mass is growing
Show answer and explanation · Link to this question
Correct answer: C
Learning point: 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. Why not the others: A — contrast CT can be justified in AKI, but it does not meet this stem's requested avoidance of iodinated contrast when an adequate MRI is immediately available. B — non-contrast CT cannot fully characterize enhancement. D — a solid mass with concerning systemic findings needs prompt evaluation. Course reading: Evidence for this case
MRI abdomen with gadobutrol (group II), day 4, creatinine 1.4: - Left kidney: 5.1-cm solid mass, heterogeneous on T2, no macroscopic fat, with avid, heterogeneous enhancement after contrast. Confined to the kidney; no extension into the renal vein or IVC; no perinephric spread; no enlarged lymph nodes. - Right kidney: 2.0-cm upper-pole cyst with simple fluid signal (dark on T1, bright on T2), hairline wall, no enhancement, no septa, no nodularity. - No adrenal lesion. No liver lesion.
CT chest without contrast, day 4: emphysema; no pulmonary nodule, no mediastinal or hilar adenopathy.
Q11The other kidney, and the follow-up
Day 6, going home: creatinine 1.3 mg/dL (1.0 six months ago, 2.3 on arrival), metformin held, the thiazide stopped, the left mass booked with urology. The 2.0-cm right cyst is thin-walled and anechoic on ultrasound, and on MRI has simple fluid signal with no enhancement, no septa and no wall thickening. What follow-up does the discharge summary order?
Image the cyst at 6 months, then yearly; recheck his creatinine only if he becomes unwell again later
Contrast CT to characterize the cyst first; a creatinine at the surgical visit; full-dose metformin from today
No cyst imaging; no kidney follow-up, because his creatinine is nearly back to his baseline of 1.0
No cyst imaging; document AKI, arrange an early renal/drug review and reassess creatinine, urine and UACR by 3 months
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Correct answer: D
Learning point: 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. Why not the others: A is the IIF schedule applied to a class I cyst, and it leaves the injured kidney unchecked; B repeats a characterization the MRI already made and restarts metformin before the eGFR is known; C gets the cyst right and treats a recovered creatinine as a recovered kidney. Course reading: Evidence for this case
Required post-session checkpoint — separate from the 37-minute live block
Answers for this section: Q12
Q12An incidental mass is not a benign diagnosis
A 63-year-old patient has intermittent painless visible hematuria and 4 kg of unexplained weight loss. Renal-protocol CT shows a 3.2-cm solid enhancing renal mass with smooth borders, no visible macroscopic fat and no enlarged nodes. The patient has no palpable mass and asks whether the scan proves this is a harmless angiomyolipoma. What is the best next step?
Schedule annual ultrasound alone because an incidental, smoothly bordered mass is presumed benign
Arrange prompt urology evaluation of a suspicious solid mass; imaging does not establish its histology
Require renal biopsy before any urology referral because every enhancing mass needs pretreatment tissue
Reassure that the absent palpable mass and nodes exclude clinically important renal malignancy
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Correct answer: B
Learning point: 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. Why not the others: A applies reassurance without establishing a benign diagnosis. C turns a selective diagnostic tool into an unnecessary prerequisite to referral. D treats absent late or uncommon findings as exclusion tests. Smooth margins and no nodes do not settle histology. Course reading: Evidence for this case
Resolution and Teaching Points
Answers for this section: Q1 · Q2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12
Urology sees him on day 5 and plans surgery once the calcium and creatinine have settled; partial versus radical nephrectomy is their call, sparing nephrons whenever the tumor allows. Oncology frames the hypercalcemia as paraneoplastic — the tumor is the gland. He goes home on day 6, oriented and walking, with the day-5 numbers holding: creatinine 1.3, corrected calcium 10.6, sodium 141. His discharge list is shorter than his admission list: atorvastatin continues; hydrochlorothiazide and excess calcium carbonate are discontinued; vitamin D is held during hypercalcemia and reconsidered later if indicated; amlodipine 5 mg daily replaces the thiazide and famotidine 20 mg daily the antacids; metformin stays held until his kidney function is known at steady state; no NSAIDs; a written sick-day rule. The discharge summary names the AKI episode, its cause, and a follow-up date.
Four weeks after the ED visit he has a left partial nephrectomy. Pathology: clear-cell renal cell carcinoma, 5.1 cm, confined to the kidney, margins negative. His PTHrP two months after surgery is 1.1 pmol/L. His calcium is 9.6.
The 3-month post-AKI visit (twelve weeks after the ED, eight weeks after surgery): BP 128/78 on amlodipine; weight 76 kg; euvolemic. Creatinine 1.4 mg/dL — now at steady state, eGFR 55 mL/min/1.73 m² by CKD-EPI 2021 (he has lost a portion of one kidney; his pre-operative creatinine was 1.2, eGFR 66). UACR 18 mg/g. Urinalysis: no blood, no protein. Calcium 9.6, sodium 140, bicarbonate 25. Medication reconciliation: metformin restarted at 500 mg twice daily with an eGFR check in three months and a plan to increase if stable; the thiazide stays off; no NSAIDs. If the eGFR is still below 60 at the next check — more than three months after surgery — he will carry a new label, CKD G3a A1; today, eight weeks after losing part of a kidney, it is a provisional stage. He also has a new habit: he has not smoked since the day of the ultrasound. Urology and oncology own the cancer surveillance. You own the kidney.
Clinical Pearl — Corrected calcium, then PTH, then the walk Correct the total calcium for albumin (0.8 mg/dL per 1 g/dL below 4.0) or measure ionized calcium. Send intact PTH first; it picks the branch. If PTH is suppressed, send the PTH-independent set together — PTHrP, 25-OH and 1,25-(OH)₂ vitamin D, SPEP/UPEP with serum free light chains, a chest film — and read the medication list for calcium, vitamin D and thiazides. A suppressed PTH does not separate milk-alkali from malignancy. The PTHrP does.
Clinical Pearl — Hypercalcemia injures the kidney twice Calcium disables the collecting duct's response to ADH (nephrogenic diabetes insipidus: polyuria, thirst, hypernatremia, a dilute urine in a dry patient) and constricts the afferent arteriole. The AKI is hemodynamic. Saline reverses both; the concentrating defect recovers over days as calcium falls. Do not read a low specific gravity as "not prerenal" when the kidney cannot concentrate.
Clinical Pearl — Saline, calcitonin, bisphosphonate — in that order, and the bisphosphonate waits for the creatinine Saline first, with reassessment. Calcitonin buys an early bridge of 48–72 hours. Prompt antiresorptive treatment supplies the durable effect in malignancy-associated hypercalcemia: select an IV bisphosphonate or denosumab with the specialist, considering renal function and hypocalcemia risk. Do not impose a blanket wait for creatinine to normalize. The loop diuretic is for volume overload during rehydration. Stop excess calcium and the thiazide, hold vitamin D during the acute evaluation, and hold metformin.
Clinical Pearl — Isomorphic red cells go to urology; dysmorphic cells go to nephrology Microhematuria is ≥3 RBC/hpf on microscopy, not a dipstick. Isomorphic cells with no protein and no casts, in a smoker over 60, are the high-risk urologic pathway: upper-tract imaging and cystoscopy. Hematuria that clears has not been explained. Never close it on a negative culture.
Clinical Pearl — Enhancement is the question; pick the dye the kidney can take today A solid renal mass usually needs contrast characterization. In AKI, weigh diagnostic benefit, alternatives and prophylaxis with radiology. An adequate MRI with a group II agent has very low NSF risk and may be a useful alternative; necessary iodinated contrast is not automatically forbidden. Bosniak I and II need no cyst surveillance, while complex lesions need their own follow-up plan.
Pitfall — Blaming the pocket before you check the gland He had every element of milk-alkali syndrome and a thiazide on his list. Students who stop at "found two benign causes" miss the tumor. The walk exists precisely for the patient with a plausible benign cause — red flags (weight loss, hematuria, a corrected calcium above 13, a mass) say keep going, and a suppressed PTH does not settle it, because milk-alkali suppresses PTH too.
Pitfall — The two-month-old hematuria that nobody owned Painless gross hematuria with isomorphic cells in a 67-year-old smoker was a urology referral the day it happened. A normal repeat dipstick and a negative culture were read as reassurance. They were neither. Intermittent bleeding is how tumors bleed.
Concept Links
Answers for this section: Q1 · Q2 · Q3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12
Assigned reading: the explanations in this case and the question-linked course evidence guide. The objective map distinguishes tested decisions from concepts taught in explanations.
Concepts: aki-03, aki-04, aki-07, aki-10, aki-26, aki-27, glom-06, lytes-10, lytes-15, lytes-16, structural-12, structural-13, structural-14, structural-15, structural-23.