Increased plasma nitric oxide, L-arginine, and arginase-1 in cirrhotic patients with progressive renal dysfunction

Zeid Kayali, Jason Herring, Pedro Baron, Edson Franco, Okechukwu Ojogho, Jason Smith, Gregory Watkins, Douglas Smith, Victor Lamin, Thanh Hoang, Rajiv Sharma, Meleah Mathahs, Lawrence Sowers, Kyle E. Brown, Warren N. Schmidt

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1030-1037
Number of pages8
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume24
Issue number6
DOIs
StatePublished - 2009
Externally publishedYes

Fingerprint

Arginase
Arginine
Nitric Oxide
Kidney
Ascites
Fibrosis
Hepatorenal Syndrome
End Stage Liver Disease
Viscera
Vasodilation
Chronic Kidney Failure
Renal Insufficiency
Multivariate Analysis
Tissue Donors
Liver
Serum

Keywords

  • Ascites
  • Cirrhosis
  • Hepatorenal syndrome
  • L-Arginine
  • Nitric oxide
  • Refractory ascites
  • Renal failure

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Cite this

Increased plasma nitric oxide, L-arginine, and arginase-1 in cirrhotic patients with progressive renal dysfunction. / 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, Lawrence; Brown, Kyle E.; Schmidt, Warren N.

In: Journal of Gastroenterology and Hepatology (Australia), Vol. 24, No. 6, 2009, p. 1030-1037.

Research output: Contribution to journalArticle

Kayali, Z, Herring, J, Baron, P, Franco, E, Ojogho, O, Smith, J, Watkins, G, Smith, D, Lamin, V, Hoang, T, Sharma, R, Mathahs, M, Sowers, L, Brown, KE & Schmidt, WN 2009, 'Increased plasma nitric oxide, L-arginine, and arginase-1 in cirrhotic patients with progressive renal dysfunction', Journal of Gastroenterology and Hepatology (Australia), vol. 24, no. 6, pp. 1030-1037. https://doi.org/10.1111/j.1440-1746.2008.05757.x
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, Lawrence ; Brown, Kyle E. ; Schmidt, Warren N. / Increased plasma nitric oxide, L-arginine, and arginase-1 in cirrhotic patients with progressive renal dysfunction. In: Journal of Gastroenterology and Hepatology (Australia). 2009 ; Vol. 24, No. 6. pp. 1030-1037.
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abstract = "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.",
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T1 - Increased plasma nitric oxide, L-arginine, and arginase-1 in cirrhotic patients with progressive renal dysfunction

AU - Kayali, Zeid

AU - Herring, Jason

AU - Baron, Pedro

AU - Franco, Edson

AU - Ojogho, Okechukwu

AU - Smith, Jason

AU - Watkins, Gregory

AU - Smith, Douglas

AU - Lamin, Victor

AU - Hoang, Thanh

AU - Sharma, Rajiv

AU - Mathahs, Meleah

AU - Sowers, Lawrence

AU - Brown, Kyle E.

AU - Schmidt, Warren N.

PY - 2009

Y1 - 2009

N2 - 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.

AB - 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.

KW - Ascites

KW - Cirrhosis

KW - Hepatorenal syndrome

KW - L-Arginine

KW - Nitric oxide

KW - Refractory ascites

KW - Renal failure

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