Hepatorenal syndrome in cirrhosis:: Pathogenesis and treatment

HRS is a major clinical event during the course of decompensated cirrhosis. Although the most characteristic feature of the syndrome is a functional renal failure caused by an intense renal vasoconstriction, it is a more generalized process affecting the heart, brain, and the splanchnic organs. There are 2 types of HRS. Type 1 HRS is characterized by a rapidly progressive impairment in circulatory and renal function. It usually develops in a closed chronological relationship with a precipitating event, particularly severe bacterial infections, superimposed acute alcoholic, toxic, or viral hepatitis, or major surgical procedures and is associated with a very poor prognosis (median survival rate, <2 weeks). Type 2 HRS is characterized by a steady impairment in circulatory and renal function. Patients with type 2 HRS have a median survival of 6 months, and their main clinical problem is refractory ascites. The pathogenesis of HRS is a deterioration in effective arterial blood volume because of a 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 IV albumin and arterial vasoconstrictors. Intrarenal mechanisms are also important and require a prolonged improvement in circulatory function to be deactivated. Vasoconstriction in the brain, muscles, and skin; increased intrahepatic vascular resistance and portal pressure; and impairment in hepatic function are other components of the syndrome. Long-term administration of IV albumin and vasoconstrictors or the correction of portal hypertension with a TIPS are effective treatments of HRS, improve the survival rate, and may serve as a bridge to liver transplantation, which is the treatment of choice in these patients.