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Question and answer links
- W1: A 66-year-old woman admitted with pneumonia has a creatinine of 0.8 mg/dL on arrival, 1.3 mg/dL at 36 hours and 1.9 mg/d · Answer
- W2: Four patients on the same ward each have a creatinine that has doubled. A cast is a cylinder of protein that formed insi · Answer
- W3: A 71-year-old man is on day 6 of gentamicin plus ampicillin for enterococcal endocarditis. His creatinine has gone from · Answer
- Q4: Patient A (Walter, 79): three days of diarrhea; BP 98/58 lying → 78/46 standing with heart rate 104 → 124; weight 74.5 k · Answer
- Q5: Walter's home list is lisinopril 20 mg daily, hydrochlorothiazide 25 mg every morning, naproxen 500 mg twice daily, metf · Answer
- Q6: Jess's urine is tea-brown. Dipstick: blood 3+, protein 1+. Microscopy: 0–1 red cells per high-power field, pigmented gra · Answer
- Q7: Jess: potassium 6.2 mEq/L with peaked T waves in V2–V4; calcium 7.1 mg/dL (corrected 6.9) with no tingling, cramps or te · Answer
- Q8: Jess weighs 66 kg, is tachycardic and mildly hypotensive, has vomited twice, and made 40 mL of dark urine in her first h · Answer
- Q9: If, from the history, orthostatics, weight loss, specific gravity 1.024 and hyaline casts, you were thinking "volume-res · Answer
- Q10: Walter, day 3, after 2 L of lactated Ringer's boluses since 21:00 last night: BP 112/70, heart rate 88, JVP 7 cm, lungs · Answer
- Q11: Walter, day 3: creatinine 3.9 mg/dL and still rising; the BMP prints "eGFR 15." The admission orders carried over metfor · Answer
- Q12: Walter, day 4: creatinine 4.4 mg/dL, K⁺ 5.8 mEq/L with a normal ECG, bicarbonate 17, urine output 25 mL/h, SpO₂ 95 % on · Answer
Session S4 · 2026-10-29 · in-session · 37 min Anchor: Acute kidney injury — acute tubular necrosis (ATN) from a prerenal/ischemic path and from rhabdomyolysis, two patients side by side · Integrates: volume assessment and fluid strategy, FENa and its limits on a diuretic, dipstick–microscopy dissociation, the electrolyte emergencies that ride with AKI (K⁺, Ca, PO₄, anion gap), the hold list and the triple whammy, drug dosing during AKI, post-AKI follow-up, the sediment map including AIN and nephrotoxic ATN One-line hook: Two patients in the same emergency department have dark urine and a creatinine that has more than doubled. They need different fluids, different drugs and different follow-up — and for one of them the clock is already running.
Learning Objectives
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12
- Stage an AKI from a creatinine trend by KDIGO 2012, and state why the printed eGFR is not valid while creatinine is moving.
- Sort an AKI into prerenal, intrinsic or post-renal from the history, exam, BMP, urine microscopy and a bladder scan, and name the first test for each compartment.
- Read the urine sediment map (hyaline → prerenal, muddy brown → ATN, white-cell casts with sterile pyuria → AIN, red-cell casts → GN) and explain what a heme-positive dipstick with no red cells means.
- Write the hold list on an AKI med-rec (NSAID first, then ACE inhibitor and thiazide, then metformin), explain the triple whammy, and dose renally cleared drugs from the creatinine trend rather than the eGFR.
- Choose a fluid strategy for a prerenal patient and for a rhabdomyolysis patient, treat hyperkalemia with an ECG change in the right order, and list the AEIOU triggers that mean "call now" (the discharge documentation and the 3-month post-AKI visit are discussed, not tested).
Warm-Up (individual commit before the case)
Answers for this section: W1 · W2 · W3
Three readiness questions: cards up, no discussion yet, and nobody's reasoning is graded from them.
W1Stage it from the trend
A 66-year-old woman admitted with pneumonia has a creatinine of 0.8 mg/dL on arrival, 1.3 mg/dL at 36 hours and 1.9 mg/dL on hospital day 3. Her urine output has stayed above 0.5 mL/kg/h throughout. Using the KDIGO 2012 criteria, what stage of AKI is she in on day 3?
Stage 1 — the rise met the 0.3 mg/dL-in-48-hours rule, and that rule defines stage 1
Stage 2 — 1.9 ÷ 0.8 = 2.4 times baseline, and the stage is set by the ratio to baseline
Stage 3 — the creatinine has more than doubled, and doubling is the stage 3 threshold
No AKI — the absolute creatinine is still under 2.0 mg/dL and the urine output never fell
Show answer and explanation · Link to this question
Correct answer: B
Learning point: 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. Why not the others: A confuses the definition rule with the staging rule. C — doubling is stage 2; tripling is stage 3. D — "under 2.0" is not a criterion anywhere; the absolute value only matters at ≥4.0. Course reading: Evidence for this case
W2The sediment map
Four patients on the same ward each have a creatinine that has doubled. A cast is a cylinder of protein that formed inside a tubule and then washed out — it tells you what was inside the tubule. Which pairing of sediment and compartment is correct?
Hyaline casts with a specific gravity of 1.025 in a patient who is dry → acute tubular necrosis
Muddy brown granular casts with a specific gravity of 1.010 after a hypotensive night → prerenal AKI
Red-cell casts with dysmorphic (misshapen) red cells and 2+ protein → acute interstitial nephritis
White-cell casts with sterile pyuria on day 10 of nafcillin → acute interstitial nephritis
Show answer and explanation · Link to this question
Correct answer: D
Learning point: 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. Why not the others: A pairs the prerenal sediment with ATN. B pairs the ATN sediment with prerenal. C pairs the glomerular sediment with an interstitial disease. Course reading: Evidence for this case
W3Day six of gentamicin
A 71-year-old man is on day 6 of gentamicin plus ampicillin for enterococcal endocarditis. His creatinine has gone from 1.1 to 1.9 mg/dL; he is still making 1.4 L of urine a day; his blood pressure is normal and he looks euvolemic. UA: fine granular casts, no white-cell casts, no blood. What is the best next step?
Stop or substitute gentamicin, check levels, and ask infectious diseases and pharmacy to individualize any further dosing
Continue gentamicin at the same dose and give a liter of saline — he is still making plenty of urine
Continue gentamicin and start furosemide to keep the urine output above 1 mL/kg/h and protect the tubules
Stop both antibiotics and start prednisone — granular casts with a new drug mean interstitial nephritis
Show answer and explanation · Link to this question
Correct answer: A
Learning point: 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. Why not the others: B — good urine output does not mean the drug is safe; non-oliguric is the usual pattern of this injury. C — a loop diuretic does not treat or prevent ATN; it only changes the urine number, and the gentamicin keeps running. D — no white-cell casts or sterile pyuria, and the timeline fits aminoglycoside ATN; steroids for AIN are nephrology's decision, not a reflex. Course reading: Evidence for this case
Part 1 — Presentation
Answers for this section: Q4 · Q5
09:00 on a Tuesday. Two patients arrive in the emergency department within an hour of each other, both with dark urine and a creatinine that has more than doubled — and almost nothing else in common.
Patient A — Walter, 79
Walter, a 79-year-old retired dairy farmer, is brought in by his daughter after three days of watery diarrhea (norovirus at his senior-center lunch group). He has kept down "some broth and crackers," is dizzy when he stands, and has not urinated since the night before. He took all of his morning pills at 07:30 — "the doctor said never skip them" — and has kept taking his over-the-counter naproxen twice a day for his knees.
Past medical history: hypertension, type 2 diabetes (A1c 7.2 %), diabetic peripheral neuropathy, knee osteoarthritis, hyperlipidemia. No heart failure; echocardiogram two years ago normal. Baseline creatinine 1.0 mg/dL three months ago at his diabetes visit (eGFR 77 mL/min/1.73 m² at steady state). Social: lives with his wife on the farm; does not smoke; two beers on Saturdays.
Vitals: T 37.4 °C · heart rate 104 · BP 98/58 lying (his clinic baseline is 142/84) · respiratory rate 16 · SpO₂ 96 % on room air · weight 74.5 kg (78.0 kg at his visit three months ago). Orthostatics: standing BP 78/46, heart rate 124, "the room spun."
Exam: tired but oriented. Dry mouth, cracked lips. Neck veins flat lying at 30°. Lungs clear. Heart regular, no murmur. Abdomen soft, mildly tender everywhere, no masses. No edema. Bladder scan: 40 mL.
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| Lisinopril | 20 mg | PO | once daily | Hypertension |
| Hydrochlorothiazide | 25 mg | PO | once daily (morning) | Hypertension |
| Naproxen (OTC) | 500 mg | PO | twice daily | Knee osteoarthritis |
| Metformin | 1,000 mg | PO | twice daily | Type 2 diabetes |
| Gabapentin | 600 mg | PO | three times daily | Diabetic peripheral neuropathy |
| Atorvastatin | 40 mg | PO | nightly | Hyperlipidemia |
Patient B — Jess, 24
Jess, a 24-year-old graduate student, collapsed at her gym late yesterday evening in a hot room after her first "Murph" — a one-mile run, 100 pull-ups, 200 push-ups, 300 air squats and another mile, in a weighted vest; she had never done more than fifty squats in a session. Within six hours both thighs were swollen and so sore she could not climb stairs, she vomited twice, and her urine turned "the color of iced tea." She took 800 mg of ibuprofen before coming in. Otherwise healthy; baseline creatinine 0.9 mg/dL at a sports physical eight months ago (eGFR 92 at steady state). Social: no alcohol this week, a caffeine pre-workout, no other supplements or drugs; last menstrual period two weeks ago.
Vitals: T 38.4 °C · heart rate 118 · BP 102/60 · respiratory rate 20 · SpO₂ 98 % on room air · weight 66 kg.
Exam: uncomfortable, alert. Mucous membranes dry. Lungs clear. Both anterior thighs are swollen, firm and exquisitely tender but compressible; pain is proportionate to the swelling, there is no pain on passive knee flexion, distal pulses are full, sensation is intact. Calves soft. Bladder scan: 60 mL. Urine hCG negative.
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| Norgestimate–ethinyl estradiol | 0.25 mg/0.035 mg | PO | once daily | Contraception |
| Ibuprofen (OTC) | 800 mg | PO | once, this morning | Muscle pain |
| Caffeine pre-workout supplement | 1 scoop (approx 300 mg caffeine) | PO | before workouts | Performance |
The first BMP on each — and the number you must not read
| Test | Walter (A), day 1 | Jess (B), hour 0 | Reference range |
|---|---|---|---|
| Creatinine (mg/dL) | 2.4 (baseline 1.0) | 2.1 (baseline 0.9) | 0.6–1.2 |
| BUN (mg/dL) | 58 | 28 | 8–20 |
| Potassium (mEq/L) | 5.4 | 6.2 | 3.5–5.0 |
| eGFR printed on the report (mL/min/1.73 m²) | "26" | "34" | ≥60 |
Clinical Pearl — "eGFR not valid — creatinine is moving" The eGFR on a BMP comes from a steady-state equation (CKD-EPI 2021): it assumes the creatinine made each day equals the creatinine cleared. While creatinine is rising, the body has not caught up — take out both kidneys and the creatinine is only about 2.0 by the next morning, while the report prints an eGFR in the 30s and the true filtration rate is zero. In AKI: ignore the printed eGFR, stage by the ratio, and follow the trend. Walter: 2.4 ÷ 1.0 = 2.4× → presumed stage 2. Jess: 2.1 ÷ 0.9 = 2.3× → presumed stage 2.
Pause — commit before the reveal
Q4Which compartment, and what confirms it?
Patient A (Walter, 79): three days of diarrhea; BP 98/58 lying → 78/46 standing with heart rate 104 → 124; weight 74.5 kg, down 3.5 kg; dry mucosa, flat neck veins, clear lungs, no edema. Creatinine 2.4 mg/dL (baseline 1.0), BUN 58, K⁺ 5.4 with a normal ECG. Urinalysis: specific gravity 1.024, bland, several hyaline casts. Bladder scan 40 mL. Which compartment is this AKI in, and what confirms it?
Intrinsic (ATN) — a BUN:creatinine ratio of 24 proves tubular injury; order a FENa and a renal ultrasound before giving any fluid
Post-renal — a 40 mL bladder scan does not exclude ureteral obstruction, so a renal ultrasound must come before any fluid
Prerenal — the history, orthostatics, concentrated urine and hyaline casts agree; give a 500 mL isotonic bolus now and reassess
Prerenal — the exam fits, but hold the fluid until the urine sodium and FENa come back, because the labs confirm the diagnosis
Show answer and explanation · Link to this question
Correct answer: C
Learning point: 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. Why not the others: A — a ratio of 24 is a prerenal clue, not proof, and ATN runs 10–15:1; nobody waits for a FENa or an ultrasound to give fluid to a hypotensive man. B — the bladder scan has excluded retention; a renal ultrasound is still ordered for unexplained AKI, but not before the bolus. D — the labs are supporting clues; the exam and the response to fluid decide. Course reading: Evidence for this case
Q5The med-rec and the hold list
Walter's home list is lisinopril 20 mg daily, hydrochlorothiazide 25 mg every morning, naproxen 500 mg twice daily, metformin 1,000 mg twice daily, gabapentin 600 mg three times daily and atorvastatin 40 mg nightly. Which set of medication orders is correct for tonight?
Hold the naproxen only; continue lisinopril because ACE inhibitors protect the kidney, and the thiazide for his pressure
Hold naproxen, lisinopril, hydrochlorothiazide and metformin; continue atorvastatin; reduce or hold gabapentin with a monitored plan
Hold lisinopril, hydrochlorothiazide and metformin; continue the naproxen so his knees do not keep him on the couch
Hold all six medicines, atorvastatin and gabapentin included, until the creatinine is back to his baseline of 1.0
Show answer and explanation · Link to this question
Correct answer: B
Learning point: 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. Why not the others: A — an ACE inhibitor protects a kidney with proteinuria over years; in a dry, hypotensive man it removes the efferent squeeze and drops filtration today. C — keeping the NSAID leaves the afferent arteriole clamped. D — holding a statin gains nothing, and gabapentin requires an individualized toxicity and withdrawal assessment rather than a blanket stop-or-continue rule. Course reading: Evidence for this case
Part 2 — Data
Answers for this section: Q6 · Q7 · Q8
Both patients' labs are back. Read them side by side.
Chemistry, hour 0
| Test | Walter (A), day 1 | Jess (B), hour 0 | Reference range |
|---|---|---|---|
| Sodium (mEq/L) | 138 | 139 | 136–145 |
| Potassium (mEq/L) | 5.4 | 6.2 | 3.5–5.0 |
| Chloride (mEq/L) | 108 | 101 | 98–107 |
| Bicarbonate (mEq/L) | 19 | 16 | 22–28 |
| Anion gap Na − (Cl + HCO₃) (mEq/L) | 138 − (108 + 19) = 11 | 139 − (101 + 16) = 22 | 8–12 |
| BUN (mg/dL) | 58 | 28 | 8–20 |
| Creatinine (mg/dL) | 2.4 (baseline 1.0) | 2.1 (baseline 0.9) | 0.6–1.2 |
| BUN:creatinine ratio | 24:1 | 13:1 | 10–20:1 |
| eGFR | not valid — creatinine is moving | not valid — creatinine is moving | — |
| Glucose (mg/dL) | 162 | 118 | 70–99 fasting |
| Calcium, total (mg/dL) | 9.0 | 7.1 | 8.5–10.5 |
| Albumin (g/dL) | 3.9 | 4.2 | 3.5–5.0 |
| Albumin-corrected calcium (mg/dL) | 9.1 | 6.9 | 8.5–10.5 |
| Ionized calcium (mmol/L) | — | 0.98 | 1.12–1.32 |
| Phosphorus (mg/dL) | 4.6 | 7.8 | 2.5–4.5 |
| Magnesium (mg/dL) | 2.0 | 2.1 | 1.7–2.4 |
| Creatine kinase, CK (U/L) | 140 | 48,000 | 30–200 |
| Uric acid (mg/dL) | 6.8 | 10.8 | 3.5–7.2 |
| AST / ALT (U/L) | 24 / 20 | 310 / 95 | <40 / <41 |
| Lactate (mmol/L) | 1.6 | 3.4 | 0.5–2.0 |
| Arterial blood gas pH / pCO₂ (mmHg) | — | 7.34 / 31 | 7.35–7.45 / 35–45 |
Jess's gas: Winter's formula predicts a pCO₂ of 1.5 × 16 + 8 = 32 ± 2 for a bicarbonate of 16, and hers is 31 — a single anion-gap metabolic acidosis, the gap filled by lactate, phosphate and organic acids from injured muscle. Albumin is normal in both patients, so the gap needs no correction.
Urinalysis, hour 0
| Urine | Walter (A), day 1 | Jess (B), hour 0 | Reference |
|---|---|---|---|
| Color | dark yellow | tea-brown | pale yellow |
| Specific gravity | 1.024 | 1.018 | 1.005–1.030 |
| pH | 5.5 | 5.5 | 4.5–8.0 |
| Protein (dipstick) | trace | 1+ | negative |
| Blood (dipstick) | negative | 3+ | negative |
| Glucose / ketones | negative / negative | negative / trace | negative |
| Leukocyte esterase / nitrite | negative / negative | negative / negative | negative |
| RBC (per hpf) | 0–2 | 0–1 | 0–2 |
| WBC (per hpf) | 0–3 | 0–2 | 0–5 |
| Casts | several hyaline | pigmented granular; no red-cell casts | none or rare hyaline |
| Urine sodium (mEq/L) | 14 | 38 | varies |
| Urine creatinine (mg/dL) | 40 | 95 | varies |
| Urine osmolality (mOsm/kg) | 750 | 600 | 50–1,200 |
Walter's FENa, with all four numbers — of the sodium the glomerulus filtered, the fraction the tubules let through: FENa = (U_Na × S_Cr) ÷ (S_Na × U_Cr) × 100 = (14 × 2.4) ÷ (138 × 40) × 100 = 33.6 ÷ 5,520 × 100 = 0.6 %. Below 1 % says "the tubules are holding sodium," the prerenal pattern. Hold that thought for Part 3.
Renal and bladder ultrasound (Walter): normal-size kidneys with preserved cortex, no hydronephrosis, post-void residual 40 mL. Jess's cause is in front of you; she had a bladder scan (60 mL) and no imaging.
ECG (Jess): sinus tachycardia 118, PR 150 ms, QRS 92 ms, peaked narrow T waves in V2–V4. ECG (Walter): sinus tachycardia 104, otherwise normal — consistent with a potassium of 5.4.
Q6Blood with no blood cells
Jess's urine is tea-brown. Dipstick: blood 3+, protein 1+. Microscopy: 0–1 red cells per high-power field, pigmented granular casts, no red-cell casts. CK 48,000 U/L. What does the mismatch between the dipstick and the microscope mean?
Glomerulonephritis — 3+ blood with casts is glomerular bleeding; send ANCA, anti-GBM and complements tonight
A contaminated or old specimen — the pad and the microscope disagree, so repeat the urinalysis before acting on either
Intravascular hemolysis — the pad is reading free hemoglobin; send LDH, haptoglobin and bilirubin before anything else
Myoglobinuria — the pad reads heme, not cells; "blood" with no red cells and a CK this high is myoglobin
Show answer and explanation · Link to this question
Correct answer: D
Learning point: 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. Why not the others: A — glomerular bleeding means red cells (dysmorphic ones) and red-cell casts under the microscope; she has neither. B — the specimen is fresh and the finding is expected, not an artifact. C — hemolysis is the other heme-without-red-cells cause, but a CK of 48,000 after a Murph settles it; no hemolysis panel comes first. Course reading: Evidence for this case
Pause — commit before the reveal
Q7The first drug for Jess
Jess: potassium 6.2 mEq/L with peaked T waves in V2–V4; calcium 7.1 mg/dL (corrected 6.9) with no tingling, cramps or tetany; phosphorus 7.8 mg/dL; bicarbonate 16 with an anion gap of 22 and a pH of 7.34. Which is the first drug, and why?
IV calcium gluconate now, for the ECG change, while insulin with dextrose and nebulized albuterol shift the potassium
IV calcium gluconate now, to correct the calcium of 7.1 before it causes tetany — the potassium can wait for a binder
IV sodium bicarbonate now, because one drug treats the acidosis and the hyperkalemia and protects the tubules
IV furosemide now, because the fastest way to lower potassium in a patient who is making urine is more urine
Show answer and explanation · Link to this question
Correct answer: A
Learning point: 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. Why not the others: B — right drug, wrong reason: the potassium is the threat tonight, and the calcium number alone is not treated. C — bicarbonate is not a reliable potassium treatment, worsens hypocalcemia, can precipitate calcium phosphate at a phosphorus of 7.8, and has no indication of its own at a pH of 7.34. D — a loop diuretic worsens perfusion in a volume-depleted patient and removes too little potassium to matter; the fluid is the removal strategy. Course reading: Evidence for this case
Q8Jess's fluid plan
Jess weighs 66 kg, is tachycardic and mildly hypotensive, has vomited twice, and made 40 mL of dark urine in her first hour. Which fluid plan is right?
Isotonic crystalloid: a 1 L bolus, then about 400 mL/h titrated to urine output of 1–3 mL/kg/h, reassessing every 2–4 hours; no routine bicarbonate or mannitol
Isotonic sodium bicarbonate infusion titrated to a urine pH above 6.5, because myoglobin precipitates in acid urine; add mannitol if output lags
A 1 L bolus, then furosemide 40 mg IV every 6 hours to keep the tubules flushed and prevent cast formation; crystalloid only to replace what the diuretic removes
Maintenance crystalloid at 75 mL/h with a recheck in the morning — a 24-year-old clears the pigment on her own, and aggressive fluid risks overload
Show answer and explanation · Link to this question
Correct answer: A
Learning point: 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. Why not the others: B — alkalinizing the urine sounds right (myoglobin precipitates below pH 5.6), but no randomized trial shows bicarbonate beats crystalloid alone, mannitol adds nothing, and bicarbonate worsens her hypocalcemia; a separate severe-acidemia indication is assessed individually rather than prescribed from a single pH cutoff. C — loop diuretics do not prevent pigment injury; they drop intravascular volume and add electrolyte trouble. D — a CK of 48,000 is massive rhabdomyolysis with a high AKI risk; maintenance fluid is under-treatment. Course reading: Evidence for this case
Part 3 — Course and Decisions
Answers for this section: Q9 · Q10 · Q11 · Q12
What happened to Walter overnight — the confounder
Walter's ED bolus was ordered at 11:00 on day 1, and the IV infiltrated. He reached the floor at 15:00 with the note "IV fluids per admitting team," and the admitting clinician, worried about "fluid overload in an elderly man," wrote for a slow drip and "reassess in the morning." Overnight his pressure was 86/48 at 01:00 and 84/50 at 04:00 (mean about 61 mmHg); the page was answered "recheck." He made 15–20 mL of urine an hour. At 09:00 on day 2 (hour 24) his creatinine was 3.1, and the team gave 500 mL and set 100 mL/h. At 21:00 on day 2 (hour 36) a rapid response for a pressure of 82/46 finally brought 1 L of lactated Ringer's, then another 1 L, and his pressure came up to 110/68. The fluids he needed at hour 2 arrived at hour 36.
One more detail surfaces on morning rounds, day 2: the nurse who collected the 09:30 urine on day 1 notes that Walter had taken his hydrochlorothiazide at 07:30 — two hours before the sample that gave the FENa of 0.6 %.
Q9Evidence update
If, from the history, orthostatics, weight loss, specific gravity 1.024 and hyaline casts, you were thinking "volume-responsive prerenal AKI" in Walter on day 1, and you then learn that his FENa of 0.6 % was drawn two hours after his morning hydrochlorothiazide, this hypothesis becomes:
Much less likely
Less likely
Unchanged
More likely
Much more likely
Show answer and explanation · Link to this question
Correct answer: D
Learning point: 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. Why not the others: A/B move away from a perfusion-related component despite supportive clinical context. C can be defensible if the learner gives substantial weight to test limitations. E gives this imperfect test excessive weight. Do not teach that only high post-diuretic values are unreliable or that a low value proves fluid responsiveness. Course reading: Evidence for this case
Walter's trend, day 1 to day 3
| Test | Day 1, 09:00 | Day 2, 09:00 | Day 3, 09:00 | Reference range |
|---|---|---|---|---|
| Creatinine (mg/dL) | 2.4 | 3.1 | 3.9 | 0.6–1.2 |
| Ratio to baseline (1.0) → KDIGO stage | 2.4× → stage 2 | 3.1× → stage 3 | 3.9× → stage 3 | — |
| BUN (mg/dL) | 58 | 60 | 60 | 8–20 |
| BUN:creatinine | 24:1 | 19:1 | 15:1 | 10–20:1 |
| Sodium (mEq/L) | 138 | 137 | 137 | 136–145 |
| Potassium (mEq/L) | 5.4 | 5.5 | 5.6 (ECG normal) | 3.5–5.0 |
| Chloride / bicarbonate (mEq/L) | 108 / 19 | 107 / 18 | 106 / 18 | 98–107 / 22–28 |
| Anion gap (mEq/L) | 11 | 12 | 13 | 8–12 |
| Urine output (mL/h, overnight average) | — | 18 | 20 (oliguria threshold for 74.5 kg = 37 mL/h) | ≥0.5 mL/kg/h |
| Weight (kg) | 74.5 | 74.8 | 77.0 | — |
| Exam | orthostatic, flat neck veins | BP 84/50 at 04:00 | BP 112/70, heart rate 88, JVP 7 cm, lungs clear, no edema | — |
| Urine | Day 1 | Day 3 | Reference |
|---|---|---|---|
| Specific gravity | 1.024 | 1.010 | 1.005–1.030 |
| Urine osmolality (mOsm/kg) | 750 | 310 | 50–1,200 |
| Casts | several hyaline | muddy brown granular casts; renal tubular epithelial cells | none or rare hyaline |
| Urine sodium (mEq/L) | 14 | 54 | varies |
| Urine creatinine (mg/dL) | 40 | 50 | varies |
| Serum sodium (mEq/L) / creatinine (mg/dL) used in the FENa | 138 / 2.4 | 137 / 3.9 | 136–145 / 0.6–1.2 |
| FENa = (U_Na × S_Cr) ÷ (S_Na × U_Cr) × 100 | (14 × 2.4) ÷ (138 × 40) × 100 = 0.6 % | (54 × 3.9) ÷ (137 × 50) × 100 = 210.6 ÷ 6,850 × 100 = 3.1 % | <1 % prerenal; >2 % ATN (with caveats) |
Pause — commit before the reveal
Q10What happened to Walter, and what is the plan now?
Walter, day 3, after 2 L of lactated Ringer's boluses since 21:00 last night: BP 112/70, heart rate 88, JVP 7 cm, lungs clear, weight 77.0 kg (74.5 on arrival), urine output 20 mL/h for ten hours. Creatinine 3.9 (2.4 → 3.1 → 3.9), BUN 60, K⁺ 5.6 with a normal ECG, bicarbonate 18. Urinalysis: specific gravity 1.010, muddy brown granular casts, tubular epithelial cells; urine Na 54 and urine creatinine 50 → FENa 3.1 %. What has happened, and what is the plan?
He is still prerenal — the oliguria means the deficit is not yet replaced; give another 2 L and keep bolusing until urine output exceeds 0.5 mL/kg/h
Prerenal AKI has become ischemic ATN: stop chasing urine output with fluid, dose drugs to the trend, no diuretic or dopamine for the kidney, call nephrology
He has developed acute interstitial nephritis from the naproxen: stop the drug, send urine eosinophils, start prednisone and recheck the creatinine in 48 hours
The FENa of 3.1 % means he was never prerenal: the day-1 orthostasis was his blood-pressure medicines, and the 36-hour fluid delay changed nothing
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Correct answer: B
Learning point: 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. Why not the others: A — chasing oliguria with fluid after the tubules have died produces pulmonary edema, not urine; "oliguria despite several liters" is a reason to reassess, not escalate. C — AIN gives white-cell casts and sterile pyuria, not muddy brown casts; urine eosinophils do not help, and steroids are not a reflex. D — the day-1 picture was prerenal; the 3.1 % is what prerenal becomes when the window closes. Course reading: Evidence for this case
Q11Re-dosing the medicines
Walter, day 3: creatinine 3.9 mg/dL and still rising; the BMP prints "eGFR 15." The admission orders carried over metformin 1,000 mg twice daily (held since day 1), gabapentin 600 mg three times daily, and enoxaparin 40 mg subcutaneously daily for VTE prophylaxis. Cockcroft–Gault on today's creatinine gives a clearance of about 16 mL/min. Which order set is correct?
Dose everything to the printed eGFR of 15: restart metformin at a reduced dose, cut the gabapentin once, and leave enoxaparin 40 mg daily alone
Change nothing today — the creatinine will come back down and every drug can follow it when it does; re-dosing now means re-dosing twice
Continue gabapentin 600 mg three times daily for his neuropathic pain, reduce the enoxaparin for his low clearance, and keep the metformin held
Keep metformin held; cut gabapentin to the low end of its renal range; reduce enoxaparin for a clearance under 30; re-dose as the trend turns
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Correct answer: D
Learning point: 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. Why not the others: A — the printed eGFR is the one number you have agreed not to read, and restarting metformin at any eGFR under 30 is contraindicated. B — "wait and see" is how a renally cleared drug reaches a toxic level. C — gets the enoxaparin and metformin right and leaves the gabapentin, the drug most likely to put a 79-year-old on the floor. Course reading: Evidence for this case
Q12When is it time to call for dialysis?
Walter, day 4: creatinine 4.4 mg/dL, K⁺ 5.8 mEq/L with a normal ECG, bicarbonate 17, urine output 25 mL/h, SpO₂ 95 % on room air, lungs clear, alert and eating breakfast. Nephrology saw him yesterday. Which statement about dialysis is correct this morning?
Urgent dialysis today — a creatinine above 4.0 mg/dL is the stage 3 threshold, and stage 3 means the kidney has failed
Urgent dialysis today — oliguria for more than 24 hours with a rising creatinine means the kidney will not recover on its own
No urgent indication today — none of the AEIOU triggers is present; treat the potassium medically and re-examine every shift
No dialysis will be needed — prerenal AKI recovers with fluid once the volume is replaced, and his neck veins are now visible
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Correct answer: C
Learning point: 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. Why not the others: A — "≥4.0" makes him stage 3, a severity label, not a dialysis indication or a verdict on recovery. B — oliguria by itself is a stage criterion and a warning, not a dialysis trigger; the question is what the oliguria is producing (overload? potassium? acid?). D — prerenal physiology that waited 36 hours became ATN, which can need dialysis; visible neck veins mean he is full now, not recovered. Course reading: Evidence for this case
Resolution and Teaching Points
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12
Jess got her calcium at hour 1 and her T waves settled within minutes. Insulin with dextrose and albuterol took the potassium to 5.4 at two hours and 5.0 at six (with glucose checks before treatment and at 30, 60, 90, 120, 180, 240, 300 and 360 minutes afterward, because hypoglycemia may be delayed), and she never needed a binder: by then she was making 150 mL of urine an hour on crystalloid titrated between 250 and 400 mL/h. Her thighs were checked every two hours for the early signs of compartment syndrome — pain out of proportion, pain on passive stretch — because the fluid that protects the kidneys can raise the pressure inside a swollen thigh; neither sign appeared. Her CK peaked at 62,000 U/L at 36 hours and fell by about half every two days; her creatinine peaked at 2.6 mg/dL on day 3 — 2.9 times baseline, still stage 2. Acetaminophen replaced the ibuprofen, and her chart says no NSAIDs until her kidney has recovered. Her calcium drifted up to 10.6 on day 6 as the muscle gave it back — expected, watched, not treated. She went home on day 7 with a creatinine of 1.3 and a written plan: no training for six weeks, then a graded return with a repeat CK, and a 3-month creatinine and urine albumin-to-creatinine ratio. At three months: creatinine 0.9, UACR 8 mg/g, blood pressure 112/70. Resolved AKI, no CKD.
Walter peaked at a creatinine of 4.6 mg/dL on day 5. Nephrology followed; he never met an AEIOU trigger, and his potassium sat at 5.6–5.8 on a low-potassium diet and a single dose of a binder. On day 7 he began making 2.5 L of urine a day — the recovery diuresis — and for two days he needed potassium and magnesium replaced rather than restricted, the trap of that phase. His creatinine was 2.6 at discharge on day 9. The discharge summary said, in a labeled paragraph: AKI stage 3, prerenal progressing to ischemic ATN, triple whammy (naproxen + lisinopril + hydrochlorothiazide) plus diarrheal volume depletion; naproxen stopped permanently; lisinopril and hydrochlorothiazide held with a deliberate restart plan; metformin held until eGFR stable ≥30; gabapentin 300 mg nightly, re-titrate as clearance recovers; enoxaparin stopped at discharge; written sick-day card given; BMP in one week; nephrology and primary care at 2 weeks; 3-month AKI follow-up booked. At two weeks his creatinine was 1.6 and his blood pressure 148/86, so lisinopril was restarted at 10 mg with a BMP a week later (K⁺ 4.9, creatinine 1.5) — protective again once he is no longer dry. The thiazide was not restarted. At three months: creatinine 1.3 mg/dL (a new baseline; eGFR 56 now that it is steady), UACR 45 mg/g, blood pressure 134/78 on lisinopril 20 mg — above the <130/80 goal, so amlodipine was added, with a BMP in one week — metformin back at full dose, gabapentin 600 mg twice daily. The label in his chart changed: CKD G3a A2 after AKI. His knees are managed with acetaminophen, topical diclofenac and a physical therapist.
Two dark urines, two stage-2 AKIs on the same morning. One was treated in the first hour and went home with a normal kidney. The other waited 36 hours and left with a chronic disease.
Clinical Pearl — "eGFR not valid — creatinine is moving" The eGFR on the BMP is a steady-state equation. In AKI it overestimates filtration, sometimes by a lot. Stage by the ratio to baseline, follow the trend, and dose drugs for a clearance lower than any estimate while creatinine is rising. Write the phrase in the note.
Clinical Pearl — Microscopy beats FENa FENa reflects sodium handling and is limited by diuretics, CKD, sepsis and timing; low values do not exclude intrinsic injury or prove fluid responsiveness. Sediment adds information but is not infallible: granular casts support tubular injury, white-cell casts can occur in interstitial inflammation, pyelonephritis or GN, and red-cell casts strongly suggest glomerular bleeding. Integrate all findings.
Clinical Pearl — Heme without red cells The dipstick blood pad reads heme, not cells. Three-plus blood with no red cells under the microscope is hemoglobin or myoglobin; the CK and the story tell you which. Tea-colored urine after a workout with a CK over 1,000 is rhabdomyolysis until proven otherwise.
Clinical Pearl — Calcium is for the ECG, not the number Give IV calcium promptly for hyperkalemic ECG toxicity, followed by potassium shifting and removal with repeat measurements. Severe hyperkalemia needs urgent monitored treatment even with a normal ECG; calcium without ECG changes follows the emergency protocol. In rhabdomyolysis avoid routine correction of asymptomatic hypocalcemia, but symptomatic hypocalcemia or severe hyperkalemia can justify calcium.
Clinical Pearl — Prerenal is a window Intact tubules concentrate urine and hold sodium; that is the whole prerenal pattern. Starve them for a night and they die, and the urine changes in front of you: specific gravity to 1.010, FENa above 2 %, casts from hyaline to muddy brown. ATN then runs on its own clock — initiation, maintenance (1–3 weeks), recovery with a diuresis — and no drug shortens it.
Pitfall — "Treating" ATN Chasing oliguria with more fluid once the tubules have died, giving furosemide to "open him up," low-dose dopamine, or routine bicarbonate for rhabdomyolysis. None of them shortens the injury. Fluid matches losses; diuretics are for genuine overload; bicarbonate is for severe acidemia on its own merits; dopamine is never.
Pitfall — Dosing to the screen Reading the printed eGFR in AKI and dosing to it — or forgetting the three drugs this case keeps returning to: metformin (hold), gabapentin (reduce), enoxaparin (adjust under a clearance of 30). Restarting the ACE inhibitor is a decision with a date and a BMP, not an accident.
Concept Links
Answers for this section: W1 · W2 · W3 · 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-01, aki-02, aki-03, aki-04, aki-05, aki-06, aki-08, aki-09, aki-11, aki-12, aki-13, aki-15, aki-22, aki-23, aki-24, aki-25, glom-01, lytes-17, lytes-19, lytes-21.
Source verification — 2026-10-12
Answers for this section: W1 · W2 · W3 · Q4 · Q5 · Q6 · Q7 · Q8 · Q9 · Q10 · Q11 · Q12
The US enoxaparin label gives 30 mg subcutaneously once daily for medical VTE prophylaxis when CrCl is below 30 mL/min. This is distinct from treatment dosing. In unstable AKI, reassess bleeding risk and prophylaxis choice with pharmacy daily. The gabapentin label uses CrCl bands; 200–700 mg once daily applies to CrCl above 15 through 29, while the 15 mL/min row is 100–300 mg daily with proportional reduction below 15. Toxicity may require holding the drug; a cautious discharge dose is not a universal renal-dose band.