ACUTE KIDNEY INJURY COMPLICATING ALCOHOL LIVER CIRRHOSIS WITH PORTAL HYPERTENSION, HIGH-TENSION ASCITES AND COMPARTMENT SYNDROME - IS THIS HEPATORENAL SYNDROME OR CONTRAST-INDUCED NEPHROPATHY?

Worsening acute injury complicating liver cirrhosis could represent an array of different etiologies, only one of which is hepatorenal syndrome. In hospitalized patients presenting with acute kidney injury against a background of liver cirrhosis, the exact determination of the mechanism of acute kidney injury is most crucial to improved patient outcomes. Whether the acute kidney injury represents hepatorenal syndrome or other causes therefore gives rise to the need for a robust diagnostic investigation. Our patient developed acute kidney injury that could have been the result of a long list of precipitating factors, other than hepatorenal syndrome.

Case Report.

A 63-yo male with a history of alcohol use disorder, opioid use disorder was diagnosed with alcohol-related liver cirrhosis in April 2025 was admitted to the medical service in mid-2025 with increasing abdominal pain and hypervolemic hyponatremia. For abdominal pain, he had contrast-enhanced abdominopelvic CT scan, a day before the admission. CT scan revealed extensive heterogeneity of the liver with large volume ascites and sequelae of portal hypertension. Hyponatremia improved with fluid restriction but despite intravenous Furosemide, he had remained hypervolemic with increasing ascites and lower extremity edema due to portal hypertension. Albumin was 2.6 g/dL. Total bilirubin was 6.7 mg/dL with mildly elevated AST (73-115) but normal ALT and raised alkaline phosphatase (152). With worsening abdominal distension from ascites, he underwent 8-liter therapeutic paracentesis. He developed post-paracentesis syndrome with acutely worsening encephalopathy that triggered the institution of oral Lactulose administration. At the same time, he had concurrently developed oliguric acute kidney injury and serum creatinine had increased from 1.03 mg/dL on hospital day 1 to 3.16 mg/dL by hospital day 5. Encephalopathy improved and by hospital day 8, he reported increasing urine output while still on PO Furosemide 80 mg BID + Spironolactone 50 mg daily. The differential diagnoses for worsening acute kidney injury included contrast-induced nephropathy, high-tension ascites with abdominal compartment syndrome, peritonitis with ascites, and hepatorenal syndrome. Ascitic fluid cultures remained negative. Serum creatinine decreased down to 1.35 mg/dL by hospital day 10 (FIGURE 1). 

Simultaneously eGFR had increased from a nadir of 21 ml/min/square m BSA on hospital day 4 to to 59 on hospital day 10 (FIGURES 2 and 3). 

The serum creatinine and eGFR trajectories, arguably, may have reflected the natural course of clear-cut contrast-induced nephropathy. At the same time, the impact of the large-volume 8-liter therapeutic paracentesis and relief of suspected compartment syndrome, however, cannot be teased out of this speculative hypothesis. There was no evidence to support peritonitis or any sepsis. Given the subsequent improvement in kidney function, arguably, there was no element of hepatorenal syndrome.

It is therefore pertinent that treating physicians must be aware that worsening acute injury complicating liver cirrhosis could represent an array of different etiologies, only one of which is hepatorenal syndrome.