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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Raised urea clearance in cirrhotic patients with high uric acid clearance is related to low salt excretion.

In cirrhotic patients without renal failure, salt retention could result from a decreased effective intravascular volume or could be a primary event leading to increased intravascular volume. Clearance of urea and uric acid depend on an effective intravascular volume. In the syndrome of inappropriate secretion of antidiuretic hormone (SIADH)--a state of increased intravascular volume--uric acid clearance is increased and that of urea is increased only when salt excretion is low. The intravascular volume of 60 consecutive cirrhotic patients without renal failure was estimated indirectly by studying the relationship between fractional excretion of filtered (FE) sodium, urea, and uric acid. Forty five per cent had a high FE uric acid (> 12%), which could mean a high intravascular volume, and presented with an FE urea that was inversely correlated with FE sodium (r = 0, 62; p < 0.001) as in SIADH, while in the controls the FE urea was positively correlated with FE sodium (r = +0, 46; p < 0.01). In patients who had a normal FE uric acid and low FE sodium (< 0.2%), the FE urea was significantly lower (40 (13)%, n = 20) than in subjects with high FE uric acid and a low FE sodium (61 (9)%, n = 16, p < 0.001); this last group also presented with lower mean blood urea concentrations (3.1 (1.2) mmol/l and 4.0 (1.8) mmol/l; p < 0.05) and a lower supine renin activity (p < 0.01). As observed in the SIADH, cirrhotic patient with high FE uric acid have raised FE urea only when salt excretion is low. It is believed that the low salt excretion is not caused by a decrease in effective intravascular volume and that this is increased in cirrhotic patients with raised FE uric acid.[1]


  1. Raised urea clearance in cirrhotic patients with high uric acid clearance is related to low salt excretion. Decaux, G., Prospert, F., Namias, B., Schlesser, M., Soupart, A. Gut (1992) [Pubmed]
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