A 58-year-old man with alcoholic cirrhosis and tense ascites is admitted with worsening abdominal girth and oliguria. Creatinine has risen from 0.9 to 2.3 mg/dL over 10 days. He is normotensive without shock, has not received nephrotoxic drugs, urine protein is negligible, and ultrasound shows no obstruction. After two days of albumin 1 g/kg/day, creatinine remains 2.2 mg/dL and urine sodium is less than 10 mEq/L. What is the most appropriate specific therapy?
- A Furosemide boluses to increase urine output
- B Terlipressin combined with intravenous albumin ✓
- C Spironolactone dose escalation to 400 mg/day
- D Immediate haemodialysis three times weekly
Explanation
These are the International Club of Ascites criteria for hepatorenal syndrome-AKI: cirrhosis with ascites, creatinine rise, lack of improvement after adequate volume expansion with albumin, absence of shock or nephrotoxins, and no structural kidney injury. Intense renal vasoconstriction drives the syndrome, so the vasopressin V1 agonist terlipressin with albumin is the accepted therapy and improves reversal rates. Diuretics worsen intravascular depletion, and dialysis offers no benefit unless bridging to transplant.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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