Treatment of Hyponatremic Cirrhosis with Ascites Resistant to Diuretics by Urea

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Abstract
We have studied the efficacy of urea in the treatment of hyponatremia and hydrosaline retention in cirrhotic patients with ascites resistant to diuretics. In 5 patients with hyponatremia and ascites resistant to a major diuretic treatment (200–400 mg spironolactone combined with 40–160 mg furosemide/day for 4 of them), urea intake (30–90 g/day) induced the following changes: the daily weight changed from a gain of 0.01 ± 0.06 kg/day to a loss of 1.03 ± 0.12 kg/day (p < 0.001) (mean ± SEM), serum sodium concentration rose from 128 ± 1.3 to 133 ± 1.4 mmol/l (p < 0.01), sodium output increased from 24 ± 4 to 82.5 ± 11 mmol/day, diuresis increased from 1.05 ± 0.10 to 2.24 ± 0.24 liters/day (p < 0.01). Despite an important weight loss, the creatinine clearance did not change significantly (53.6 ± 4.5 ml/min before and 70.0 ± 8.2 ml/min during urea). In patients responding to classical diuretics, urea as a monotherapy was less effective. From the 6 patients with resistant ascites, only 1 developed prerenal uremia after urea treatment. In order to enhance urea efficacy, it is important to take it together with a long-loop diuretic. Intermittent urea intake seemed to be useful in cirrhotic patients with hyponatremia associated with ascites resistant to diuretics and with low or normal blood urea concentrations.