Hepatorenal syndrome (HRS) is a serious event during the course of decompensated cirrhosis. Although the most characteristic feature of the syndrome is a functional renal failure due to intense renal vasoconstriction, it is a more generalized process affecting the heart, brain and splanchnic organs. There are two types of HRS. Type 1 HRS is characterized by a rapidly progressive impairment of the circulatory and renal functions associated with a very poor prognosis (median survival rate lower than 2 weeks). Type 2 HRS is characterized by a steady impairment of the circulatory and renal functions with a median survival of 6 months. The pathogenesis of HRS is a deterioration of the effective arterial blood volume due to splanchnic arterial vasodilation and a reduction in venous return and cardiac output. It is therefore not surprising that the syndrome can be reversed by the simultaneous administration of intravenous albumin and arterial vasoconstrictors. Intrarenal mechanisms are important as well and require prolonged improvement of the circulatory function to be deactivated. Long-term administration of intravenous albumin and vasoconstrictors or correction of portal hypertension with a transjugular intrahepatic portacaval shunt are effective treatments of HRS, and many serve as a bridge to liver transplantation, the treatment of choice in these patients.

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