Hepatorenal syndrome: historical perspectives on the recognition of the problem. Review

Abstract

Hepatorenal syndrome (HRS) is a severe functional complication of portal hypertension and liver cirrhosis, characterized by profound renal hemodynamic dysfunction in the absence of significant structural kidney damage and associated with high mortality. Recent studies report a 90‑day mortality of 40 – 60%, depending on disease severity and therapeutic interventions. The pathophysiology of HRS is primarily driven by marked splanchnic vasodilation, resulting in reduced effective arterial blood volume, renal vasoconstriction, and a decline in glomerular filtration rate. The association between advanced liver disease and renal dysfunction was first recognized in the 19th century, whereas a clear clinical definition of HRS emerged in the mid‑20th century. Subsequent advances led to the classification of HRS into two major types: type I, an acute, rapidly progressive form with a very poor prognosis, and type II, a more indolent form commonly associated with refractory ascites. Therapeutic strategies focus on restoring effective arterial circulation. The most evidence‑based pharmacological treatment is the combination of vasoconstrictors, particularly terlipressin, combined with albumin. Invasive approaches, including transjugular intrahepatic portosystemic shunt (TIPS), peritoneovenous shunting, albumin‑based extracorporeal liver support systems, and renal replacement therapy, are considered as supportive or bridging options in selected patients, especially those awaiting liver transplantation. Prevention of HRS is based on early infection control, avoidance of nephrotoxic agents, adequate correction of hypovolemia, and routine administration of albumin after large‑volume paracentesis. Overall, HRS represents a hallmark of advanced hepatic decompensation and requires early recognition and a multidisciplinary therapeutic approach.