Hepatorenal Syndrome Without Avid Sodium Retention

Abstract

A urinary sodium concentration [U(Na)] of less than 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 greater than 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 other patients who had hepatorenal syndrome and a U(Na) consistently less than 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 less than 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 similar in both groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal failure after upper gastrointestinal bleeding in cirrhosis: Incidence, clinical course, predictive factors, and short-term prognosis

“…Thus, some patients with cirrhosis and renal failure caused by ATN may have low urine sodium, whereas patients with cirrhosis and renal failure as a result of causes other than ATN may have high urine sodium. [16][17][18] Likewise, the use of markers of tubular damage in the differential diagnosis of renal failure in cirrhosis may be misleading, because some patients with hepatorenal syndrome may have high concentrations of urinary enzymes. 19,20 In other patients in the current study, renal failure after gastrointestinal bleeding was probably related to the presence of severe bacterial infections.…”

Advances in the pathogenesis and treatment of type-1 and type-2 hepatorenal syndrome

“…However, acute tubular necrosis in patients with cirrhosis and ascites usually courses with oliguria, low urine sodium concentration and urine osmolality greater than plasma osmolality [11]. On the contrary, relatively high urinary sodium concentration has been exceptionally observed in patients with HRS [12].…”

Hepatorenal syndrome: an update

“…In some cases, urinary sodi um may be present at a concentration of more than 20 mEq/l, with the presence or absence of acute tubular necrosis. 38 Urinary osmolarity is generally greater than plasma osmolarity and in most cases there is no hematuria, which is an indication that there is no glomerular lesion.…”