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Increased plasma nitric oxide, L‐arginine, and arginase‐1 in cirrhotic patients with progressive renal dysfunction
Author(s) -
Kayali Zeid,
Herring Jason,
Baron Pedro,
Franco Edson,
Ojogho Okechukwu,
Smith Jason,
Watkins Gregory,
Smith Douglas,
Lamin Victor,
Hoang Thanh,
Sharma Rajiv,
Mathahs Meleah,
Sowers Lawrance,
Brown Kyle E,
Schmidt Warren N
Publication year - 2009
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2008.05757.x
Subject(s) - medicine , ascites , renal function , hepatorenal syndrome , cirrhosis , gastroenterology , nitric oxide , liver disease , portal hypertension , endocrinology , endothelial dysfunction
Background and Aims: Increased levels of nitric oxide (NO) are hypothesized to contribute to renal dysfunction in patients with decompensated cirrhosis. In this study, we examined whether splanchnic and/or peripheral NO levels and L‐arginine (L‐Arg) correlate with progressive renal dysfunction in cirrhotics. Methods: Serum NO metabolites (NOx) and L‐Arg were measured in: controls ( n = 10); organ donors ( n = 12); compensated cirrhotics ( n = 17), cirrhotics with ascites ( n = 25), refractory ascites ( n = 11) or hepatorenal syndrome type II (HRS) ( n = 11) and chronic renal failure patients ( n = 18). Results: Plasma NOx and L‐Arg levels rose progressively with worsening renal function in decompensated cirrhotics. Both NOx and L‐Arg levels were highest in patients with HRS ( P < 0.001 and P < 0.025, respectively). While there were no differences in NOx levels related to the site of sampling, L‐Arg levels were lowest in hepatic venous blood. There were significant relationships of NOx and L‐Arg with Model for End‐Stage Liver Disease score and Child–Pugh scores ( P < 0.04 and P < 0.01, respectively). Multivariate analysis showed a significant relationship between NOx, L‐Arg and HRS. Conclusion: Worsening renal function in decompensated cirrhosis is accompanied by progressive elevation in plasma NOx and L‐Arg. These findings support the hypothesis that NO‐mediated vasodilation is probably linked with the mechanism of progressive renal failure in decompensated cirrhotics.