Ascites and hepatorenal syndrome in cirrhosis: pathophysiological basis of therapy and current management

Abstract

Ascites is the most common complication of cirrhosis [1,2]. It develops late during the course of the disease, when there is severe portal hypertension and hepatic insufficiency. Not surprisingly, it is associated with a poor survival [3] (50% mortality rate within 3 years, Fig. 1). The development of ascites is, therefore, a clear indication for liver transplantation. There are several studies indicating that parameters estimating systemic hemodynamics and renal function are better predictors of survival than those estimating hepatic function [4–6]. The prognosis of patients with dilutional hyponatremia, refractory ascites and hepatorenal syndrome (HRS) is extremely poor and liver transplantation should be indicated prior to the development of these complications [3,7]. Other parameters with prognostic value in cirrhotic patients with ascites are mean arterial pressure, plasma renin activity, plasma norepinephrine concentration, urinary sodium excretion, the renal ability to excrete free water, liver size, serum bilirubin, serum albumin concentration, and prothrombin time [8,9]. The current article is focused on the treatment of ascites and HRS in cirrhosis. To provide the reader with the rationale of the therapeutic measures used in patients with cirrhosis and ascites or HRS, the pathophysiology of these complications is briefly reviewed. The role of liver transplantation in the management of decompensated cirrhotic patients with ascites is not included in this review. 2. The pathophysiological basis of therapy of ascites and HRS