eNOS 894T allele can contribute to endothelial dysfunction but not QT interval prolongation in dialytic patients

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Medical & Clinical Research
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Background: Cardiovascular complications are common in chronic kidney disease (CKD) patients. Endothelial nitric oxide synthase (eNOS) is very important for the homeostasis of the cardiovascular system, and its gene polymorphism at position 894 (G>T) has not been investigated with QTc interval in patients on dialysis. Objective: This study evaluated the association of the 894G>T polymorphism with QTc prolongation and endothelial dysfunction risk in dialysis patients. Methods: Predialysis blood samples were collected for eNOS gene polymorphism, nitric oxide (NO), thiobarbituric acid reactive substances (TBARS), total antioxidant, asymmetric dimethylarginine (ADMA) and L-arginine, and 12-lead electrocardiograms were analyzed in these patients. Statistics were based on continuous and categorical variables using Fisher’s exact or Chi-square or one-way ANOVA or Kruskal- Wallis tests. The results were considered significant when P < 0.05. Results: The study showed that the GG genotype was prevalent, with 54% of patients, followed by 41% GT and 6% TT, and the genotypic distribution was not associated with QTc prolongation. Furthermore, patients with the T allele showed increased ADMA, L-arginine and peroxidation lipid levels with reduced NO synthesis. Conclusion: Our study showed a lack of association between QTc interval and eNOS polymorphism; however, it was found that patients with the T allele had a greater risk of developing endothelial dysfunction by ADMA, which could contribute to future cardiovascular complications and worsening of CKD.

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ANDRADE, JESSICA L.F.; NOGUEIRA, GUILHERME B.; BELLINI, MARIA H.; MANCUSO, FREDERICO; KLEINE, JOAO P.; SILVA, ISMAEL D.C.G.; PUNARO, GIOVANA R.; HIGA, ELISA M.S. eNOS 894T allele can contribute to endothelial dysfunction but not QT interval prolongation in dialytic patients. Medical & Clinical Research, v. 5, n. 11, p. 291-297, 2020. DOI: 10.33140/MCR.05.11.01. Disponível em: http://repositorio.ipen.br/handle/123456789/31807. Acesso em: 30 Dec 2025.
Esta referência é gerada automaticamente de acordo com as normas do estilo IPEN/SP (ABNT NBR 6023) e recomenda-se uma verificação final e ajustes caso necessário.

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