Abstract
Hepatorenal syndrome (HRS) is a life-threatening complication of advanced liver disease, especially cirrhosis. It involves functional kidney failure without structural damage. The main cause is severe splanchnic vasodilation from portal hypertension, which reduces effective blood volume. This triggers compensatory vasoconstriction, leading to reduced kidney perfusion. HRS is classified into two types. Type 1 is rapid and often triggered by infection or bleeding. Type 2 progresses slowly and is linked to refractory ascites. Diagnosis is clinical and requires ruling out shock, nephrotoxins, and kidney disease. Early diagnosis is vital due to its high mortality. We describe the case of a male patient, age 54, with a history of alcohol-induced cirrhosis. He had laboratory evidence of acute kidney injury, oliguria, hyponatremia, and progressive fatigue. Ultrasound showed a nodular liver with ascites, indicating cirrhosis and portal hypertension. Both kidneys retained their normal size and corticomedullary differentiation, ruling out intrinsic renal disease. Type 1 HRS was identified after all other possible causes of renal dysfunction were ruled out. Renal function partially improved after the patient received intravenous albumin and terlipressin. He was then referred to be evaluated for a liver transplant. This case highlights how complex the clinical and diagnostic aspects of HRS can be while also emphasizing the critical need for early detection and treatment. By combining sonographic findings, such as indicators of portal hypertension, with clinical and biochemical data, we can make a more informed diagnosis of HRS. Although pharmacological treatments may provide temporary relief, liver transplantation remains the gold standard for ensuring long-term survival in patients with advanced liver disease complicated by HRS.