Hepatorenal syndrome overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sunny Kumar MD [2], Mehrian Jafarizade, M.D [3]
Overview
Hepatorenal syndrome (HRS) refers to acute renal failure that occurs in the setting of cirrhosis or fulminant liver failure associated with portal hypertension, usually in the absence of other disease of the kidney. It is a direct result of changes in the splanchnic and systemic circulation from cirrhosis or fulminant hepatic failure. It is usually secondary to trigger events which cause multi-system organ failure.
Historical Perspective
Historically, the hepatorenal syndrome was first defined as acute renal failure that occurred in the setting of biliary surgery. The syndrome was soon associated with advanced liver disease. It was determined that kidneys transplanted from patients with hepatorenal syndrome were functional, leading to the hypothesis that hepatorenal syndrome was a systemic process as opposed to renal disease, which affects the renal function.
Classification
The classification of hepatorenal syndrome is based on the deteriorating function of kidney in to two types: type 1 rapidly progressive and type 2 HRS, slowly progressive.
Pathophysiology
The major pathophysiologic mechanism responsible for the clinical manifestation of hepatorenal syndrome is renal vasoconstriction. The hemodynamic disturbances include increased cardiac output, systemic vasodilatation and low arterial blood pressure. Thus, renal vasoconstriction occurs even with a normal blood volume and increased cardiac output.