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Question and answer links
- W1: In decompensated cirrhosis three findings travel together — a urine sodium below 10 mEq/L, a falling serum sodium and a · Answer
- W2: FENa — the fraction of filtered sodium that ends up in the urine — is context dependent. In which patient is it most use · Answer
- Q3: Dennis: creatinine 2.2 mg/dL (0.9 three weeks ago), BP 96/58 lying and 80/50 standing, weight down 3 kg, temperature 37. · Answer
- Q4: Day 1 orders for Dennis: alert, no asterixis; sodium 124 mEq/L; potassium 5.8 mEq/L with a normal ECG; ascitic neutrophi · Answer
- Q5: If, on admission, you were thinking "volume-responsive prerenal AKI" — a man dried out by two diuretics, poor eating and · Answer
- Q6: Day 3: Dennis meets the HRS-AKI criteria (creatinine 0.9 → 2.7 mg/dL; no improvement in the 24 hours after his volume wa · Answer
Session S4 · 2026-10-29 · supplementary · 20 min Anchor: Acute kidney injury — hepatorenal syndrome (HRS): recognition and the stepwise approach · Integrates: hypervolemic hyponatremia, diuretic and spironolactone hyperkalemia, FENa limits, NSAID avoidance, the infection search (spontaneous bacterial peritonitis) One-line hook: In a man with cirrhosis, a FENa of 0.3 % says "prerenal — give fluid" whether or not fluid will help. The test that answers the question is doing the right things and watching what the creatinine does once the volume is back.
Learning Objectives
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6
- Explain why a low urine sodium and FENa cannot separate volume depletion, NSAID injury and hepatorenal syndrome in cirrhosis, and state the diuretic caveat.
- Run the exclusion steps before the word "hepatorenal": stop diuretics, spironolactone and NSAIDs; tap the ascites; image for obstruction; look for bleeding; replace volume only if it was lost.
- Treat hypervolemic hyponatremia and spironolactone hyperkalemia without saline and without overshooting the sodium.
- Recognize HRS-AKI by the current criteria and name the next step — a specialist decision on a vasoconstrictor with albumin, and a transplant evaluation.
- Counsel a patient with cirrhosis on lifelong NSAID avoidance and a safe analgesic (discussed, not tested).
Warm-Up (individual commit before the case)
Answers for this section: W1 · W2
Two readiness questions. Commit to an answer before you open each reveal.
W1One mechanism, three findings
In decompensated cirrhosis three findings travel together — a urine sodium below 10 mEq/L, a falling serum sodium and a creeping creatinine — while the patient carries liters of extra salt and water as ascites and edema. Which single mechanism explains all three?
The diuretics: furosemide and spironolactone pull sodium out of the body, which lowers the serum sodium and dries out both kidneys
Tense ascites presses on both ureters, so urine backs up and the kidneys can no longer excrete enough sodium, water or creatinine
Splanchnic vasodilation underfills the arteries; RAAS, sympathetic tone and ADH respond: sodium and water held, renal arteries clamped
Ammonia from the failing liver poisons the tubules directly, so they can no longer excrete enough sodium, water or creatinine each day
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Correct answer: C
Learning point: 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. Why not the others: A can contribute to volume loss but does not unify the cirrhotic physiology; B is not the usual mechanism; D does not explain the findings. Diuretic exposure and tubular injury do not prevent a low urine sodium in cirrhosis. Course reading: Evidence for this case
W2When can a FENa be read?
FENa — the fraction of filtered sodium that ends up in the urine — is context dependent. In which patient is it most useful to help distinguish volume-responsive AKI from tubular injury?
A 66-year-old man with heart failure who took furosemide 80 mg this morning and whose creatinine rose overnight
A 70-year-old woman, oliguric after two days of diarrhea, on no diuretic and with a normal baseline creatinine
A 58-year-old man with CKD G4 whose creatinine rose from 2.6 to 3.4 mg/dL after a week of poor intake
A 47-year-old woman in septic shock from pneumonia whose creatinine has doubled within the last 24 hours
Show answer and explanation · Link to this question
Correct answer: B
Learning point: 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. Why not the others: A — a diuretic forces sodium into the urine, so a high value cannot be read (a low one despite the diuretic still means sodium avidity). C — CKD raises the baseline FENa, so prerenal AKI can read above 1 %. D — sepsis can give a low FENa despite tubular injury. Course reading: Evidence for this case
Part 1 — Presentation
Answers for this section: Q3
Dennis is a 59-year-old retired electrician with alcohol-related cirrhosis, diagnosed two years ago when his belly first filled with fluid (ascites); he has not had a drink in 14 months. A week ago he cracked a molar. Waiting for a dental appointment, he has taken over-the-counter ibuprofen, three 200-mg tablets four times a day, and lived on soup because chewing hurts. He kept taking his water pills every morning at 07:00 "to keep the belly down." For three days he has been lightheaded on standing and his belly has felt fuller and sore; today he has hardly urinated. He arrived in the emergency department at 14:00.
Past history: cirrhosis with ascites (two large-volume paracenteses this year); no bleeding; no known kidney disease. Creatinine 0.9 mg/dL at his hepatology visit three weeks ago, weight 83.0 kg, BP 112/70. Social: lives with his wife; former smoker.
Vitals: T 37.8 °C · heart rate 104 · BP 96/58 lying · respiratory rate 18 · SpO₂ 96 % on room air · weight 80.0 kg. Standing: BP 80/50, heart rate 122, lightheaded.
Exam: alert and oriented; no asterixis (the flapping tremor of hepatic encephalopathy). Yellow sclerae, spider angiomas, red palms. Dry mouth; neck veins flat at 30°. Lungs clear. Abdomen distended with shifting dullness (moderate ascites) and mild tenderness everywhere, no guarding. 1+ ankle edema. Rectal: brown stool, guaiac negative. Bladder scan: 60 mL.
| Drug | Dose | Route | Frequency | Indication |
|---|---|---|---|---|
| Furosemide | 40 mg | PO | once daily (07:00) | Ascites |
| Spironolactone | 100 mg | PO | once daily (07:00) | Ascites |
| Ibuprofen (OTC) | 600 mg | PO | four times daily for 7 days | Toothache |
| Thiamine | 100 mg | PO | once daily | Nutrition after alcohol use |
First results (blood 14:30; urine 19:00)
| Test | Result | Reference range |
|---|---|---|
| Creatinine (mg/dL) | 2.2 (0.9 three weeks ago) | 0.6–1.2 |
| Ratio to baseline → KDIGO stage | 2.2 ÷ 0.9 = 2.4× → presumed stage 2, given the acute history | — |
| eGFR | not valid — creatinine is moving | — |
| BUN (mg/dL) | 34 | 8–20 |
| Sodium (mEq/L) | 124 | 136–145 |
| Potassium (mEq/L) | 5.8 | 3.5–5.0 |
| Hemoglobin (g/dL) | 10.8 (11.0 three weeks ago) | 13.5–17.5 |
| Urinalysis | amber; specific gravity 1.021; bilirubin 2+; trace protein; no blood, leukocyte esterase or nitrite; 0–2 RBC and 0–2 WBC/hpf; a few hyaline casts; no granular casts or tubular cells | — |
| Urine sodium (mEq/L) | 8 | varies |
| Urine creatinine (mg/dL) | 48 | varies |
| Urine output since arrival | about 30 mL/h | ≥0.5 mL/kg/h (40 mL/h at 80 kg) |
The three-week-old baseline alone does not establish a seven-day rise. The acute history supports presumed AKI; seek intervening results and follow the trajectory. The admitting note reads: "FENa 0.3 % — prerenal." The arithmetic is right: FENa = (U_Na × S_Cr) ÷ (S_Na × U_Cr) × 100 = (8 × 2.2) ÷ (124 × 48) × 100 = 17.6 ÷ 5,952 × 100 = 0.3 %. The urine was collected twelve hours after his morning furosemide.
Q3The first orders
Dennis: creatinine 2.2 mg/dL (0.9 three weeks ago), BP 96/58 lying and 80/50 standing, weight down 3 kg, temperature 37.8 °C, mild diffuse abdominal tenderness, ibuprofen 2,400 mg a day for 7 days, both diuretics this morning, bladder scan 60 mL, bland urine, FENa 0.3 %. Which first set of orders is best?
Read the FENa of 0.3 % as volume-responsive prerenal AKI: 2 L of 0.9 % saline over four hours, both diuretics at half dose so the ascites cannot return, recheck in the morning
Read the low urine sodium as hepatorenal syndrome: a vasoconstrictor with albumin tonight, and no paracentesis because he has no real fever and no rebound tenderness at all
Stop only the ibuprofen; keep furosemide and spironolactone running for the ascites; tap the abdomen if the fever or pain worsens; recheck the creatinine in 48 hours
Stop furosemide, spironolactone and ibuprofen; diagnostic paracentesis tonight; renal ultrasound; cautious balanced crystalloid for volume loss with prompt reassessment; add albumin if specifically indicated
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Correct answer: D
Learning point: 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. Why not the others: A assigns fluid responsiveness from FENa and continues diuretics; B labels HRS before the assessment and misses possible SBP; C delays indicated evaluation and continues volume-depleting therapy. Crystalloid is not inherently forbidden in a cirrhotic patient who has lost volume. Course reading: Evidence for this case
Part 2 — Data
Answers for this section: Q4 · Q5
Initial balanced crystalloid was given with reassessment. The paracentesis returned by 20:00 with the results below; ceftriaxone and SBP-directed albumin were started that evening.
| Test | Result | Reference range |
|---|---|---|
| Sodium (mEq/L) | 124 | 136–145 |
| Potassium (mEq/L) | 5.8 | 3.5–5.0 |
| Chloride (mEq/L) | 96 | 98–107 |
| Bicarbonate (mEq/L) | 20 | 22–28 |
| Anion gap, Na − (Cl + HCO₃) (mEq/L) | 124 − (96 + 20) = 8; albumin-corrected 8 + 2.5 × (4.0 − 2.6) = 11.5 | 8–12 |
| BUN : creatinine | 34 : 2.2 = 15 : 1 | 10–20 : 1 |
| Albumin (g/dL) | 2.6 | 3.5–5.0 |
| Total bilirubin (mg/dL) | 3.4 | 0.2–1.2 |
| INR | 1.7 | 0.9–1.1 |
| AST / ALT (U/L) | 64 / 30 | <40 / <41 |
| WBC (× 10⁹/L) | 9.6 | 4.0–11.0 |
| Platelets (× 10⁹/L) | 78 | 150–400 |
| Ascitic fluid neutrophils (PMN, cells/µL) | 420; Gram stain: no organisms; culture pending | SBP at ≥250 |
ECG: sinus tachycardia at 102; normal PR and QRS; no peaked T waves. Renal and bladder ultrasound: kidneys 11.4 and 11.8 cm with normal cortex, no hydronephrosis; bladder 60 mL; small nodular liver, moderate ascites, spleen 15 cm.
Two numbers deserve a second look. The BUN:creatinine ratio is only 15: a failing liver makes less urea, so "above 20 means prerenal" does not apply. And the baseline creatinine of 0.9 flattered him — wasted muscles make little creatinine — so a rise to 2.2 is a bigger loss of filtration than it looks.
Q4The order that should not be written
Day 1 orders for Dennis: alert, no asterixis; sodium 124 mEq/L; potassium 5.8 mEq/L with a normal ECG; ascitic neutrophils 420/µL, Gram stain negative; temperature 37.8 °C; albumin running. Which order should NOT be written?
IV ceftriaxone now for the ascitic neutrophil count of 420/µL, without waiting for the culture result or a higher fever
0.9 % saline at 150 mL/h until the sodium reaches 135 mEq/L, to treat the hyponatremia and the creatinine together
Spironolactone kept off, a low-potassium diet, potassium rechecked in 6 hours, and no IV calcium for a normal ECG
After correcting volume depletion, consider free-water restriction for persistent dilutional hyponatremia; limit sodium rise to 8 mEq/L per 24 hours
Show answer and explanation · Link to this question
Correct answer: B
Learning point: 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. Why not the others: A treats SBP at a PMN count ≥250 without awaiting culture; C removes contributors and monitors moderate hyperkalemia, escalating if potassium or ECG worsens; D applies restriction only after correcting depletion, with a safe correction limit. Course reading: Evidence for this case
Forty-eight hours later
By day 3 every reversible piece has been dealt with. The diuretics and ibuprofen have been off since the first evening. By day 2 the albumin had refilled his arteries: he is no longer orthostatic, his neck veins are visible at 30°, his lungs are clear and his SpO₂ is 96 % on room air. Ceftriaxone has run since day 1; he has been afebrile since day 2, his belly is no longer tender, and the ascitic culture grew E. coli sensitive to ceftriaxone.
Q5Evidence update
Concordance-style practice — no expert panel stands behind the key. "Unchanged" means the finding does not move the hypothesis.
If, on admission, you were thinking "volume-responsive prerenal AKI" — a man dried out by two diuretics, poor eating and an NSAID — and you then learn that 48 hours after those drugs stopped, with albumin given until he was no longer orthostatic and his SBP treated, his creatinine has gone 2.2 → 2.4 → 2.7 mg/dL with a urine sodium still at 6 mEq/L, this hypothesis becomes:
Much less likely
Less likely
Unchanged
More likely
Much more likely
Show answer and explanation · Link to this question
Correct answer: A
Learning point: 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. Why not the others: B is defensible if the learner retains mixed injury and delayed creatinine kinetics; C–E do not account for the lack of response. The degree of probability change remains formative. Course reading: Evidence for this case
| Test | Day 1 (admission) | Day 2 (24 h) | Day 3 (48 h) | Reference range |
|---|---|---|---|---|
| Creatinine (mg/dL) | 2.2 | 2.4 | 2.7 | 0.6–1.2 |
| Ratio to baseline (0.9) → KDIGO stage | 2.4× → 2 | 2.7× → 2 | 3.0× → 3 | — |
| BUN (mg/dL) | 34 | 36 | 38 | 8–20 |
| Sodium (mEq/L) | 124 | 125 | 126 | 136–145 |
| Potassium (mEq/L) | 5.8 | 5.1 | 4.7 | 3.5–5.0 |
| BP lying → standing, mmHg (standing heart rate) | 96/58 → 80/50 (122) | 102/60 → 98/58 (96) | 104/62 → 100/60 (88) | — |
| Urine output (average) | about 30 mL/h | about 30 mL/h | about 25 mL/h | ≥40 mL/h at 80 kg |
| Urine sodium (mEq/L) | 8 (on diuretics) | — | 6 (48 h off diuretics) | varies |
| Urine creatinine (mg/dL) | 48 | — | 70 | varies |
| FENa | 0.3 % (drawn on a diuretic) | — | (6 × 2.7) ÷ (126 × 70) × 100 = 0.2 % | see W2 |
| Sediment | bland; a few hyaline casts | — | bland; no granular casts or tubular cells | — |
Part 3 — Course and Decisions
Answers for this section: Q6
HRS-AKI in plain words (the 2024 ADQI–ICA criteria, summarized in the HRS handout): cirrhosis with ascites; AKI by the KDIGO creatinine or urine-output rules; no improvement within 24 hours of adequate resuscitation when it was needed (Dennis was refilled by day 2 and worse on day 3); and no stronger explanation as the main cause — no shock, no nephrotoxin still running, no obstruction, no sediment pointing to glomerulonephritis or ATN (some tubular injury can coexist). There is no absolute creatinine threshold, and a routine 48-hour albumin course is no longer required.
Q6What happens next
Day 3: Dennis meets the HRS-AKI criteria (creatinine 0.9 → 2.7 mg/dL; no improvement in the 24 hours after his volume was restored, with diuretics and NSAID stopped; SBP treated; no shock, no obstruction, bland sediment). He is alert, SpO₂ 96 % on room air, lungs clear, potassium 4.7 mEq/L. What is the next step?
Start hemodialysis today, because a creatinine that has tripled despite treatment means his kidneys will not recover on their own
Two more days of IV albumin at a higher dose, because a urine sodium of 6 mEq/L shows he is still volume-depleted
Call hepatology and nephrology today for a monitored vasoconstrictor-with-albumin decision and a liver-transplant evaluation
Restart furosemide and spironolactone to clear the reaccumulating ascites now that the infection is treated, and refer him for TIPS
Show answer and explanation · Link to this question
Correct answer: C
Learning point: 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. Why not the others: A — dialysis treats AEIOU complications, which he does not have, and in HRS it is a bridge, not a reflex. B — more albumin into a refilled man risks pulmonary edema; the low urine sodium is the clamped kidney, not a dry one. D — the diuretics are part of what you removed, and TIPS is not a routine rescue for HRS-AKI. Course reading: Evidence for this case
Resolution and Teaching Points
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6
Hepatology and nephrology started a vasoconstrictor with albumin that afternoon on a monitored unit, with continuous oxygen saturation; on day 5 he was up 2 kg and the albumin was cut back. His creatinine turned on day 4 — 2.7, 2.5, 2.1, 1.7 — and was 1.4 mg/dL on day 9. He finished the ceftriaxone, hepatology started long-term SBP prophylaxis, his sodium reached 131 mEq/L without rising more than 3 in a day, and the transplant team met him before discharge.
The NSAID got its own conversation. In cirrhosis with ascites the kidney depends on prostaglandins to hold its inflow arterioles open, so a week of ibuprofen pulled away the prop that was keeping filtration up. He left with a written banned list — ibuprofen, naproxen, aspirin for pain, ketorolac, and the "PM" and cold remedies that hide them — and one safe analgesic: acetaminophen, no more than 2 g a day. Hepatology restarted his diuretics at lower doses a week later, with a BMP three days after and a sodium diet under 2 g a day. Four weeks out his creatinine was 1.2 mg/dL — and with his muscle mass, even that flatters him.
Clinical Pearl — A low FENa in cirrhosis is a description, not a diagnosis The cirrhotic kidney clings to sodium in volume depletion, NSAID injury, hepatorenal syndrome and early tubular injury alike; on a diuretic the cut-offs do not apply at all. The sediment, the drug list and the response to volume do the sorting.
Clinical Pearl — Tap the belly Every patient with cirrhosis and ascites admitted with AKI gets a diagnostic paracentesis, fever or not. Ascitic neutrophils ≥250/µL make the diagnosis of SBP, and antibiotics start then — not when the culture returns.
Clinical Pearl — HRS-AKI is diagnosed by a test of time Stop the diuretics, spironolactone and NSAIDs; treat infection; replace volume only if it was lost; reassess. No improvement within 24 hours of adequate resuscitation, with no stronger explanation, is HRS-AKI — and the next move is a call, not a prescription.
Clinical Pearl — No NSAIDs, ever, with cirrhosis and ascites The cirrhotic kidney is prostaglandin-dependent. Write the banned list, name the combination products, and give a safe alternative: acetaminophen up to 2 g a day.
Pitfall — Saline for the sodium Hypervolemic hyponatremia is too much water, not too little salt. Volume-depleted patients still need appropriate resuscitation; a fixed saline drip aimed only at normalizing sodium risks overload and osmotic demyelination in the patients most prone to it — alcohol use, liver disease, malnutrition.
Pitfall — Calling HRS too early, or never Labeling HRS before tapping the belly and stopping the NSAID treats the wrong disease; pouring albumin for days into a refilled patient delays the specialist treatment and floods the lungs.
Concept Links
Answers for this section: W1 · W2 · Q3 · Q4 · Q5 · Q6
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-05, aki-20, aki-23, htn-cardiorenal-26, lytes-07, lytes-14, structural-20.