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Abstract Hepatorenal syndrome (HRS) is a potentially reversible syndrome occurring in patients with cirrhosis, ascites and liver failure. It is characterized by impaired renal function, marked alterations in the cardiovascular function and over- activity of the endogenous vasoactive systems. Marked vasoconstriction in the kidney causes low glomerular filtration rate (GFR), whereas in the systemic circulation, there is decreased vascular resistance due to splanchnic and peripheral arterial vasodilatation. A similar syndrome can also occur in acute liver failure and acute alcoholic hepatitis Studies have demonstrated that the annual incidence of HRS was estimated at 8% to 40% in cirrhosis Types of Hepatorenal syndrome: Type 1: Cirrhosis with rapidly progressive renal failure. Type 2: Cirrhosis with subacute renal failure. Type 3: Cirrhosis with types 1 or 2 HRS superimposed on chronic kidney disease or acute renal injury. Type 4: Fulminant liver failure with HRS. Pathogenesis : The etiopathogenesis of HRS has not been fully resolved and there are possible theories to explain it at cellular and molecular levels. The defining feature of HRS is profound vasoconstriction of the renal vasculature due to inadequate blood flow to the kidneys. The culmination of several factors leads to the development of HRS: (1) portal hypertension; (2) altered peripheral blood circulation; (3) activation of the sympathetic nervous system; and (4) the release of chemical mediators |