[Hepatorenal syndrome]

Abstract

Hepatorenal syndrome is complication of the advanced cirrhosis characterized by functional renal failure and changes of systemic blood pressure due to increased activity of endogenous vasoactive systems. Functional renal failure is due to severe renal cortical ischemia and reduction of glomerular filtration rate (GFR) developing in the late stages of cirrhosis. The pathogenesis of hepatorenal syndrome is the result of an extreme underfilling of the arterial circulation secondary to arterial vasodilatation located in the splanchnic circulation. Reduced effective arterial blood volume triggers a compensatory response with activation of systemic and renal vasoconstrictor systems. At the same time, the ascites becomes refractory in some patients, as it is no longer responsive to diuretic treatment. These changes result from combination of deteriorating liver function and increasing portal pressure, further splanchnic vasodilatation, increase of circulating vasoconstrictors, and decrease of renal blood flow and GFR. Hepatorenal syndrome can be precipitated by shock, infection, nephrotoxic drugs, bleeding, surgery or large volume paracentesis. Renal failure may be rapidly progressive (type I HRS) or may develop more slowly (type II HRS), which is usually associated with refractory ascites. The diagnosis of HRS is based on established diagnostic criteria aimed at excluding the nonfunctional causes of renal failure. The prognosis of patients with HRS is very poor. Liver transplantation remains the only curative treatment for the time being. Pharmacological therapies based on the use of vasoconstrictor drugs may serve as a bridge to liver transplantation. Prevention of HRS by albumin infusion is recommended in patients with spontaneous bacterial peritonitis and by pentoxifylline in patients with the acute alcoholic hepatitis.