Abstract
IntroductionThe hepatorenal syndrome (HRS) is defined as a potentially reversible kidneyfailure in patients with liver cirrhosis and ascites. In its physiopathology, hyperactivity of the sympathetic and renin-angiotensin aldosterone systems (RAAS), elevation of nitric oxide, and systemic vasodilatation are determinant factors [1]. Recently, a cardiomyopathic component associated with HRS has been reported [2]. HRS is classified into two types. In type I, there is a rapid elevation of serum creatinine, at least twice the normal range, which reflects a reduction of creatinine clearance of 50%, usually reaching levels of up to 2.5mg/dL. HRS type II has a more insidious and less aggressive course, and its hallmark is ascites refractory to diuretics. HRS type I generally courses with oliguria (less than 400–500 mL/day) and is secondary to infections or metabolic disturbances. About half of the patients usually respond to the therapies currently used [3]. Cirrhotic cardiomyopathy (CMP) is now a well-established condition, defined as the presence of blunted ventricular response to stress, in cirrhotic patients, with a raised basal cardiac output accompanied by systolic, diastolic, electrophysiological, structural, histological, and biochemical changes [4, 5]. Recent studies have stated myocardial dysfunction in cirrhosis as a contributing factor, or even a precipitant, of HRS [2].