Plasma levels of brain natriuretic peptide in patients with cirrhosis

✍ Scribed by Giorgio La Villa; Roberto Giulio Romanelli; Vincenzo Casini Raggi; Cristina Tosti-Guerra; Maria Laura De Feo; Fabio Marra; Giacomo Laffi; Paolo Geñtilini

• Publisher: John Wiley and Sons
• Year: 1992
• Tongue: English
• Weight: 693 KB
• Volume: 16
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840160126

✦ Synopsis

Plasma levels of brain natriuretic peptide, a recently identified cardiac hormone with natriuretic activity, were measured in 11 healthy subjects, 13 cirrhotic patients without ascites, 18 nonazotemic cirrhotic patients with ascites and 6 patients with cirrhosis, ascites and functional kidney failure. Plasma levels of brain natriuretic peptide were similar in healthy subjects and cirrhotic patients without ascites (5.56 f 0.65 and 7.66 f 0.68 fmol/ml, respectively). In contrast, cirrhotic patients with ascites, with and without functional kidney failure, had significantly higher plasma concentrations of brain natriuretic peptide (19.66 k 1.37 and 16.00 k 1.91 fmollml, respectively) than did healthy subjects and patients without ascites (p c 0.01); no significant difference was found between the two groups of cirrhotic patients with ascites with respect to this parameter. In the whole group of cirrhotic patients included in the study, brain natriuretic peptide level was directly correlated with the degree of impairment of liver and kidney function, plasma renin activity and plasma levels of aldosterone and atrial natriuretic peptide. The results of this study indicate that brain natriuretic peptide is increased in cirrhotic patients with ascites and suggest that sodium retention in cirrhosis is not due to deficiency of this novel cardiac hormone. (HEPATOLOGY 1992;16:156-161.) Deficient production of an endogenous natriuretic factor is traditionally considered a possible mechanism contributing to sodium retention in cirrhosis (1-2). However, several studies have shown that plasma levels of atrial natriuretic peptide (ANP) are not reduced in patients with cirrhosis and ascites but are rather normal (3-4) or increased (5-9), ruling out the possibility that sodium retention in cirrhosis could be due to a deficiency of this natriuretic factor. We (10) and others (11) recently obtained indirect evidence suggesting that