Journals / Balkan Medical Journal / 2016 / Cilt: 33 - Sayı: 2

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

Pages
128–137
Publication Date
2022-10-11
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Thus, the reduction of ADMA and SDMA concentrations might play a protective role in ESRD patients.

📌 3 Key Takeaways

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Objective & Hypothesis:Background: Chronic kidney diseases are known to influence nitric oxide metabolites (NOx) and asymmetric dimethylarginine (ADMA), though the exact mechanism is still poorly understood.
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Key Findings & Data: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.
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Conclusion & Impact:Thus, the reduction of ADMA and SDMA concentrations might play a protective role in ESRD patients.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

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 Glu- 298Asp 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.

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Cite This Article

İLHAN, N., ÇELİKER, H., KAMAN, D., ATEŞ, K. (2022). eNOS Glu298Asp Polymorphism and Endothelial Dysfunction in Patients with and without End-stage Renal Disease. Balkan Medical Journal, Cilt: 33 - Sayı: 2, 128–137. https://ajindex.com/articles/461305

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References (3)

  1. Nakamura T, Sato E, Fujiwara N, Kawagoe Y, Ueda Y, Suzuki T, et al. Positive association of serum levels of advanced glycation end products and high mobility group box-1 with asymmetric dimethylarginine in nondiabetic chronic kidney disease patients. Metabolism 2009;58:1624-8. [CrossRef] Förstermann U. Oxidative stress in vascular disease: causes, de- fense mechanisms and potential therapies. Nat Clin Pract Car- diovasc Med 2008;5:338-49. [CrossRef] Harrison DG. Cellular and molecular mechanisms of endothelial cell dysfunction. J Clin Invest 1997;100:2153-7. [CrossRef] Jackson P, Loughrey CM, Lightbody JH, McNamee PT, Young IS. Effect of hemodialysis on total antioxidant capacity and serum antioxidants in patients with chronic renal failure. Clin Nephrol 1995;44:1135-8.
  2. Daschner M, Lenhartz H, Botticher D, Schaefer F, Wollschlager M, Mehls O, et al. Influence of dialysis on plasma lipid peroxidation prod- ucts and antioxidant levels. Kidney Int 1996;50:1268-72. [CrossRef] Paradossi U, Ciofini E, Clerico A, Botto N, Biagini A, Colom- bo MG. Endothelial function and carotid intimamedia thick- ness in young healthy subjects among endothelial nitric ox- ide synthase Glu298Asp and T-786C polymorphisms. Stroke 2004;35:1305-9. [CrossRef] Naber CK, Baumgart D, Altmann C, Siffert W, Erbel R, Heusch G. eNOS 894T allele and coronary blood flow at rest and during adenosineinduced hyperemia. Am J Physiol Heart Circ Physiol 2001;281:1908-12.
  3. Hsu CN, Huang LT, Lau YT, Lin CY, Tain YL. The combined ratios of L-arginine and asymmetric and symmetric dimethylar- ginine as biomarkers in spontaneously hypertensive rats. Transl Res 2012;159:90-8. [CrossRef] Busch M, Fleck C, Wolf G, Stein G. Asymmetrical (ADMA) and symmetrical dimethylarginine (SDMA) as potential risk factors for cardiovascular and renal outcome in chronic kidney disease - possible candidates for paradoxical epidemiology? Amino Acids 2006;30:225-32. [CrossRef] Lu TM, Chung MY, Lin CC, Hsu CP, Lin SJ. Asymmetric di- methylarginine and clinical outcomes in chronic kidney disease. Clin J Am Soc Nephrol 2011;6:1566-72. [CrossRef] Szlachcic A, Krzysiek-Maczka G, Pajdo R, Targosz A, Magi- erowski M, Jasnos K, et al. The Impact of Asymmetric Dimeth- ylarginine (ADMA), the Endogenous Nitric Oxide (NO) Syn- thase Inhibitor, to the Pathogenesis of Gastric Mucosal Damage. Curr Pharm Des 2013;19:90-7. [CrossRef] Young JM, Terrin N, Wang X, Greene T, Beck GJ, Kusek JW, et al. Asymmetric dimethylarginine and mortality in sta