Association of endothelial nitric oxide synthase gene polymorphisms with end-stage renal disease: a systematic review and meta-analysis

Zhu, Yun; Yuping, Yang; Tong, Zongwu; Sun, Yang; Yang, Fang; Sun, Fuchun

doi:10.3109/0886022x.2014.900601

Cited by 14 publications

(13 citation statements)

References 44 publications

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“…NOS produces the nitric oxide (NO) from L‐arginine. Renal tubular epithelial cells and the mesangial cells generate NO, which mainly regulates renal hemodynamic and tubular function . The NOS might play important roles in the cyst growth and hypertension in ADPKD .…”

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confidence: 99%

Effects of endothelial nitric oxide synthase gene on end stage renal disease progression in autosomal dominant polycystic kidney disease

et al. 2014

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Effects of endothelial nitric oxide synthase gene on end stage renal disease progression in autosomal dominant polycystic kidney disease

et al. 2014

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“…Bradykinin B 2 receptor ( B 2 R ) and the endothelial nitric oxide synthase ( eNOS) genes have been proven to be candidate genes associated with ESRD [5,6]. Meta analysis studies showed that the candidate genes involved in the development of ESRD led to contradictory results in various populations [7]. This may be due to the difference of genetic predisposition causing this association of polymorphism with ESRD to differ between populations.…”

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confidence: 99%

Analysis of Human Bradykinin Receptor Gene and Endothelial Nitric Oxide Synthase Gene Polymorphisms in End-Stage Renal Disease Among Malaysians

Ramachandran

Ismail

Jaafar

et al. 2014

Balkan Journal of Medical Genetics

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The aim of this study was to determine the association of the c.894G>T; p.Glu298Asp polymorphism and the variable number tandem repeat (VNTR) polymorphism of the endothelial nitric oxide synthase (eNOS) gene and c.181C>T polymorphism of the bradykinin type 2 receptor gene (B2R) in Malaysian end-stage renal disease (ESRD) subjects.A total of 150 ESRD patients were recruited from the National Kidney Foundation’s (NKF)dialysis centers in Malaysia and compared with 150 normal healthy individuals. Genomic DNA was extracted from buccal cells of all the subjects. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was carried out to amplify the products and the restricted fragments were separated by agarose gel electrophoresis. Statistical analyses were carried out using software where a level of p <0.05 was considered to be statistically significant.The genotypic and allelic frequencies of the B2R gene (c.181C>T, 4b/a) and eNOS gene (c.894G>T) polymorphisms were not statistically significant (p >0.05) when compared to the control subjects. The B2R and eNOS gene polymorphisms may not be considered as genetic susceptibility markers for Malaysian ESRD subjects.

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“…Although some changes may be in terms of allele frequency for this polymorphism because of different ethnic groups, we found that the T allele distribution of this polymorphism similar to Caucasians (27) and other studies conducted in Turkey (21) and (41). Furthermore, several studies were shown that the eNOS gene could play a major role in the diabetic nephropathy and Glu298Asp polymorphisms in the eNOS gene were associated with ESRD susceptibility (19,20,42).…”

Section: Glu298asp Polymorphism and Esrdmentioning

confidence: 99%

“…This variant has been found to be connected with hypertension, diabetic nephropathy, ESRD and nondiabetic ESRD (14)(15)(16). Accordingly, the increase of plasma ADMA levels during CKD has suspected to be a factor in the progression of CKD (17)(18)(19)(20).…”

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eNOS Glu298Asp Polymorphism and Endothelial Dysfunction in Patients with and without End-stage Renal Disease

et al. 2016

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Background: Chronic kidney diseases are known to influence nitric oxide metabolites (NOx) and asymmetric dimethylarginine (ADMA), though the exact mechanism is still poorly understood. Aims: The purpose of the present study was to examine eNOS Glu298Asp gene polymorphism, plasma NOx and ADMA concentration in subjects with and without End-stage Renal Disease. Study Design: Case-control study. Methods: In this study, genotype distributions of Glu298Asp in exon 7 of the eNOS gene polymorphisms in 130 hemodialysis and 64 peritoneal dialysis patients were compared with 92 controls. NOx was measured by using the Griess reaction while arginine, ADMA and SDMA measurements were performed by HPLC. Genotyping for eNOS Glu298Asp polymorphism was detected with the polymerase chain reaction and/or polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results: When the genotype frequencies of TT and GT genes were compared between both groups, there was no detected statistically important difference, eventhough a TT genotype frequency was 27 (20.8%) versus 17 (26.6%), GT heterozygote genotype frequency was 52 (40%) versus 22 (34.4%), and GG homozygote genotype frequency was 51 (39.2%) versus 25 (39.1%), respectively (p>0.05). NOx, SDMA and ADMA concentrations were significantly elevated in subjects with hemodialysis patients as compared to their corresponding controls. Whereas nitrite was found to be significantly decreased in the patient with peritoneal dialysis. Conclusion: Not observed any connection between the Glu298Asp polymorphism in the eNOS gene and end-stage Renal Diseases in our study population under different dialysis treatments. However, higher ADMA and SDMA concentrations in subjects with ESRD support the existing hypothesis that NOx overproduction affects endothelial dysfunction. Thus, the reduction of ADMA and SDMA concentrations might play a protective role in ESRD patients. Keywords: eNOS Glu298Asp, endothelial dysfunction, end-stage renal disease Endothelial dysfunction and impaired regulation of nitric oxide (NO) system has emerged as the characteristics of chronic kidney diseases (CKD). The accumulation of asymmetric dimethylarginine (ADMA) plays a role in the impairment regulation of NO in these patients; however, the mechanism of these disorders is not clear. Increased levels of ADMA and NO bioavailability reduction play a vital role in the pathogenesis of many diseases like coronary atherosclerosis, CKD or diabetes mellitus (1). Morever, accumulation of reactive oxygen species by the increasing NO leads to atherogenesis, hence a over production may also damage cells and tissues (2).Oxidative stress has a very considerable role in the endothelial dysfunction, vascular damage and in the development of cardiovascular diseases. Some of these mechanisms are associated with the oxidative inactivation of NO production and the inhibition of NO synthase activity by free oxygen radicals

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Association of endothelial nitric oxide synthase gene polymorphisms with end-stage renal disease: a systematic review and meta-analysis

Cited by 14 publications

References 44 publications

Effects of endothelial nitric oxide synthase gene on end stage renal disease progression in autosomal dominant polycystic kidney disease

Effects of endothelial nitric oxide synthase gene on end stage renal disease progression in autosomal dominant polycystic kidney disease

Analysis of Human Bradykinin Receptor Gene and Endothelial Nitric Oxide Synthase Gene Polymorphisms in End-Stage Renal Disease Among Malaysians

eNOS Glu298Asp Polymorphism and Endothelial Dysfunction in Patients with and without End-stage Renal Disease

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