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.
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 failurepatients (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.
Authors: Arlin B Blood; Hobe J Schroeder; Michael H Terry; Jeanette Merrill-Henry; Shannon L Bragg; Kurt Vrancken; Taiming Liu; Jason L Herring; Lawrence C Sowers; Sean M Wilson; Gordon G Power Journal: Circulation Date: 2011-01-31 Impact factor: 29.690
Authors: Yomna I Ibrahim; Janet R Ninnis; Andrew O Hopper; Douglas D Deming; Amy X Zhang; Jason L Herring; Lawrence C Sowers; Timothy J McMahon; Gordon G Power; Arlin B Blood Journal: J Pediatr Date: 2011-09-09 Impact factor: 4.406
Authors: Marek Saracyn; Tomasz Ząbkowski; Robert Zdanowski; Marek Brytan; Janusz Patera; Zbigniew Nowak; Grzegorz Kade; Zofia Wańkowicz Journal: Med Sci Monit Date: 2014-09-27
Authors: Marek Saracyn; Janusz Patera; Janusz Kocik; Marek Brytan; Robert Zdanowski; Arkadiusz Lubas; Wojciech Kozłowski; Zofia Wańkowicz Journal: Arch Med Sci Date: 2012-07-04 Impact factor: 3.318