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

Kayali, Zeid; Herring, Jason; Baron, Pedro; Franco, E; Ojogho, Okechukwu; Smith, Jason C.; Watkins, G L; Smith, D. P.; Lamin, Victor; Hoang, Thanh D.; Sharma, Rajiv; Mathahs, M. Meleah; Sowers, Lawrance; Brown, Kyle E.; Schmidt, Warren N.

doi:10.1111/j.1440-1746.2008.05757.x

Cited by 20 publications

(17 citation statements)

References 53 publications

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“…In a study conducted by Kayali et al, NO levels were found to be increased in cirrhotic patients with renal dysfunction, and the highest levels were observed in patients with HRS. One of the notable findings in this study was the fact that L-arginine levels were increased in these patients [16]. …”

Section: Discussionmentioning

confidence: 98%

Association of eNOS Gene Polymorphisms G894T and T-786C with Risk of Hepatorenal Syndrome

Seçkin

Yiğit

Yeşilada

et al. 2016

Gastroenterology Research and Practice

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Background. There are no studies investigating the relationship between endothelial nitric oxide synthase (eNOS) gene polymorphisms and hepatorenal syndrome (HRS). Aim. The purpose of this study is to elucidate whether eNOS gene polymorphisms (G894T and T-786C) play a role in the development of type-2 HRS. Methods. This study was carried out in a group of 92 patients with cirrhosis (44 patients with type-2 HRS and 48 without HRS) and 50 healthy controls. Polymorphisms were determined by polymerase chain reaction (PCR) and melting curve analysis. Results. We did not find any significant difference in allele and genotype distributions of the eNOS -T-786C polymorphism among the groups (p = 0.440). However, the frequency of GT (40.9%) and TT (13.6%) genotypes and mutant allele T (34.1%) for the eNOS G894T polymorphism were significantly higher (p < 0.001 and p < 0.001, resp.) in the HRS group than in both the stable cirrhosis (14.6%, 4.2%, and 11.5%, resp.) and the control (22.0%, 2.0%, and 13.0%, resp.) groups. Conclusion. The occurrence of mutant genotypes (GT/TT) and mutant allele T in eNOS -G894T polymorphisms should be considered as a potential risk factor in cirrhotic patients with HRS.

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Section: Discussionmentioning

confidence: 98%

Association of eNOS Gene Polymorphisms G894T and T-786C with Risk of Hepatorenal Syndrome

Seçkin

Yiğit

Yeşilada

et al. 2016

Gastroenterology Research and Practice

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“…Plasma arginine concentrations were measured using an isotope-dilution gas chromatograph/mass spectrometry (GC/MS) method as previously described [16]. …”

Section: Methodsmentioning

confidence: 99%

Inhaled Nitric Oxide Therapy Increases Blood Nitrite, Nitrate, and S-Nitrosohemoglobin Concentrations in Infants with Pulmonary Hypertension

Ibrahim

Ninnis

Hopper

et al. 2012

The Journal of Pediatrics

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Objective To measure the circulating concentrations of nitric oxide (NO) adducts with NO bioactivity following inhaled NO therapy in infants with pulmonary hypertension. Study design In this single center study five sequential blood samples were collected from infants with pulmonary hypertension before, during and after therapy with iNO (n=17). Samples were collected from a control group of hospitalized infants without pulmonary hypertension (n=16) and from healthy adults for comparison (n=12). Results After beginning iNO (20 ppm) whole blood nitrite increased about two-fold within two hours (P<0.01). Whole blood nitrate increased to four-fold higher than baseline during treatment with 20ppm iNO (P<0.01). S-nitrosohemoglobin (SNO-Hb) increased measurably after beginning iNO (P<0.01) whereas iron nitrosyl hemoglobin and total Hb-bound NO-species compounds did not change. Conclusion Treatment of pulmonary hypertensive infants with iNO results in increases in nitrite, nitrate, and SNO-Hb in circulating blood. We speculate that these compounds may be carriers of NO bioactivity throughout the body and account for peripheral effects of iNO in the brain, heart and other organs.

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“…Furthermore, a patient with liver cirrhosis and hepatocellular carcinoma without any other risk factors has been reported (Tsang et al 2012). Variable degrees of hepatic cirrhosis also occur in other UCDs (LaBrecque et al 1979;Mori et al 2002), and increased levels of l-arginine have been observed in patients with liver cirrhosis with progressive loss of renal function (Kayali et al 2009). …”

Section: Clinical Characteristicsmentioning

confidence: 97%

Hyperargininemia due to arginase I deficiency: the original patients and their natural history, and a review of the literature

et al. 2015

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Hyperargininemia is caused by deficiency of arginase 1, which catalyzes the hydrolysis of L-arginine to urea as the final enzyme in the urea cycle. In contrast to other urea cycle defects, arginase 1 deficiency usually does not cause catastrophic neonatal hyperammonemia but rather presents with progressive neurological symptoms including seizures and spastic paraplegia in the first years of life and hepatic pathology, such as neonatal cholestasis, acute liver failure, or liver fibrosis. Some patients have developed hepatocellular carcinoma. A usually mild or moderate hyperammonemia may occur at any age. The pathogenesis of arginase I deficiency is yet not fully understood. However, the accumulation of L-arginine and the resulting abnormalities in the metabolism of guanidine compounds and nitric oxide have been proposed to play a major pathophysiological role. This article provides an update on the first patients ever described, gives an overview of the distinct clinical characteristics, biochemical as well as genetical background and discusses treatment options.

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

Abstract: 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.

Cited by 20 publications

References 53 publications

Association of eNOS Gene Polymorphisms G894T and T-786C with Risk of Hepatorenal Syndrome

Association of eNOS Gene Polymorphisms G894T and T-786C with Risk of Hepatorenal Syndrome

Inhaled Nitric Oxide Therapy Increases Blood Nitrite, Nitrate, and S-Nitrosohemoglobin Concentrations in Infants with Pulmonary Hypertension

Hyperargininemia due to arginase I deficiency: the original patients and their natural history, and a review of the literature

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