Abstract

Hepatorenal syndrome (HRS) is a unique form of severe functional kidney failure due to intense renal vasoconstriction that develops in patients with cirrhosis in the absence of significant histological abnormalities of the kidneys. 1,2 Detailed discussions of the pathophysiology of HRS and the diagnostic approach to HRS are presented in two other articles in this issue of Clinical Liver Disease and can also be found elsewhere. 1,2 The diagnosis of HRS is essentially a process of excluding other causes of kidney failure. Therefore, the identification of objective parameters that can be used in the differential diagnosis between HRS and other causes of kidney failure in patients with cirrhosis is of the utmost importance. Recent studies suggest that the measurement of the neutrophil gelatinase-associated lipocalin concentration in urine, a biomarker of tubular damage, may be of value in the differential diagnosis between HRS and other causes of acute kidney failure in patients with cirrhosis, but information is still limited. 3,4 The current diagnostic criteria for HRS have been reported elsewhere. 5 There are two types of HRS corresponding to the severity and progression of kidney failure (Table 1). Type 1 HRS is associated with rapidly progressive kidney failure and a very low survival expectancy, the median survival time being only 2 weeks if it is not treated; type 2 HRS is associated with stable or slowly progressive kidney failure and has a better prognosis than type 1 HRS. 1,2

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