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Hepatorenal syndrome without avid sodium retention

A urinary sodium concentration [U(Na)] of <10 mmoles per liter is considered important in differentiating hepatorenal syndrome from other causes of progressive renal impairment in patients with liver disease. However, occasionally, patients with hepatorenal syndrome have been recognized in whom the U(Na) is consistently >10 mmoles per liter. Eight such patients, in all of whom there was no clinical or laboratory evidence to implicate other causes of progressive renal impairment, were identified. The clinical features, hepatic and renal status and hospital course were compared with eight otherpatients who had hepatorenal syndrome and a U(Na) consistently <10 mmoles per liter. The mean U(Na) was 24 ± 4 mmoles per liter in the high U(Na) group and 3.7 ± 1.8 mmoles per liter in the low U(Na) group. All patients in both groups had acutely decompensated alcoholic hepatitis of similar severity and activity. The high U(Na) group had significantly less clinical ascites and peripheral edema and higher serum levels of sodium and chloride both at the onset of the hepatorenal syndrome and throughout the clinical course. Significant differences in the serum potassium and blood urea nitrogen levels became apparent between the two groups of patients as renal failure progressed, and the mean average blood urea nitrogen to serum creatinine ratio was significantly higher (p < 0.025) in the low U(Na) group (13.8 ± 0.9 vs. 10.1 ± 1.1). Mean urinary potassium concentration was significantly higher in the high U(Na) patients but urinary creatinine concentrations, specific gravity and sediment were similarin both groups of patients. Three of the patients from the high U(Na) group came to autopsy. In all, the only renal histological abnormality was reflux of proximal convolutedtubular epithelium into Bowman's capsule, a finding consistent with hepatorenal syndrome. It is concluded that, in patients with acute alcoholic hepatitis, a U(Na) >10 mmoles per liter does not exclude the diagnosis of hepatorenal syndrome. It is suggested that the clinical and biochemical differences between patients with the hepatorenalsyndrome and a high or low U(Na) can be explained by variations in the proximal tubularabsorption of sodium.