Hepatorenal Syndrome

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Abstract
The first description of disturbances in renal function in chronic liver diseases was made by Frerichs and Flint in two independent reports from the late nineteenth century (2). These reports described the development of oliguria in patients with chronic liver disease in the absence of proteinuria and with a normal renal histology, and proposed the first pathophysiologic interpretation of HRS by linking the abnormalities of renal function to the disturbances present in the systemic circulation. The detailed clinical description of HRS, however, was not made until the 1950s in studies by Sherlock, Papper, and Vessin (2,3). These studies emphasized the functional nature of renal failure, the coexistence of abnormalities in the systemic circulation, and the poor prognosis of the syndrome. Investigations performed in the 1960s and 1970s, particularly those by Epstein (4), demonstrated that renal failure in HRS is due to an extreme vasoconstriction of the renal circulation and paved the way for a large number of studies assessing the role of vasoactive substances in the pathogenesis of renal hypoperfusion in HRS. Relevant among these investigations are those implicating the renin-angiotensin system, the sympathetic nervous system, and renal prostaglandins (5). Important recent contributions include the description of a strong association between bacterial infections, especially spontaneous bacterial peritonitis, and the development of HRS in patients with cirrhosis and the use of vasopressin analogues in the management of HRS (6,7,8). Finally, the proposal of the arterial vasodilation hypothesis of ascites formation and the recent Consensus Conference on Definition and Diagnostic Criteria of Hepatorenal Syndrome represent key contributions to the recent history of HRS that have stimulated markedly the clinical research in this field (1,9).

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