ROLE OF T-786C ENDOTHELIAL GENE POLYMORPHISM OF NO - SYNTHASE IN THE DEVELOPMENT OF ACUTE CONTRAST-INDUCED NEPHROPATHY IN PATIENTS WITH CORONARY HEART DISEASE

  • Sagynbaeva G. A. Department of Faculty Therapy, The Kyrgyz State Medical Academy named after I.K. Akhunbaev, Kyrgyzstan, Bishkek
  • Kaliev R. R. Doctor of Medical Sciences, Professor, Department of Faculty Therapy, The Kyrgyz State Medical Academy named after I.K. Akhunbaev, Kyrgyzstan, Bishkek
Keywords: gene polymorphism, nitric oxide, chronic renal failure, endothelial dysfunction, сontrast-induced nephropathy

Abstract

Contrast-induced nephropathy (CIN) is the third considerable cause of acute kidney injury (AKI) and makes up almost 10% of all acute kidney failure (AKF) cases.
Objective. To study the role of polymorphism of eNOS-gene in the development of acute contrast-induced nephropathy (CIN) in case of coronary heart disease.
Materials and methods. The prospective study was conducted in the National Cardiology and Therapy Center named after academician Mirsaid Mirahimov from 2015 to 2018. A total of 184 patients with coronary heart disease (CHD) aged 33-70 years (average age 55.2 ± 8.5 years) were examined to determine possible associative relationships between eNOS gene polymorphism (T786C) and the development of acute CIN. Of these, the group without CIN was 152, and with the CIN there were 32 patients who underwent coronary angiographic examination (CAG). Radiopaque contrast agents Ultravist (Iopromide) and Omnipack (Iohexol) were used. CIN was defined as an increase in serum creatinine (Scr) concentration by more than 25% from the initial level or by more than 0.5 mg/dL (44.2 μmol/L) and a decrease in glomerular filtration rate (GFR) after administration of an iodinated contrast agent within 48-72 hours in the absence of other reasons. A molecular genetic study was conducted to determine the T-786C polymorphism of the eNOS gene.
Results. The genotype frequency of the TT gene in the group with CIN was 87.5%, and in the group without CIN 69.7%, the reliability was p <0.05. But the connection of acute CIN with the genotypes of TS and SS was not observed in both of the groups.
Conclusions. TT genotype T-786C polymorphism of the eNOS gene is a risk factor for the development of acute contrast-induced in patients with coronary heart disease.

References

Berns A.S. Nephrotoxicity of contrast media. Kidney Int. 1989; 36:730-740;

Rich M.W., Crecelius C.A. Incidence, risk factors, and clinical course of acute renal insufficiency after cardiac catheterization in patients 70 years of age or older. A prospective study. Arch. Intern. Med. 1990; 150: 1237-1242.

Andreucci M., Solomon R., Tasanarong A. Side effects of radiographic contrast media: pathogenesis, risk factors and prevention. BioMed Research International. Volume 2014, Article ID 741018, 1- 20 pages. http://dx.doi.org/10.1155/2014/741018

Gleeson T. G., Bulugahapitiya S. Contrast-induced nephropathy. American Journal of Roentgenology. 2004;183(6):1673–1689.

Nash K., Hafeez A., Hou S. Hospital acquired renal insufficiency Am. J. Kidney Dis. – 2002. – Vol. 39. – P. 930–936

Mehran R., Aymong E.D., Nikolsky E. et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J. Am. Coll.Cardiol. 2004; 44: 1393-1399.

Bartholomev B.A., Harjai K.J., Dukkipati S. et al. Impact of nephropathy after percutaneous coronary intervention and a metod for risk stratification. Am. J. Cardiol. 2004; 93:1515-1519.

Forstermann U., Closs E. I., Pollock J. S. et al. Nitric oxide synthase isozymes: characterization, purification, molecular cloning, and functions. Hypertension 1994; 23: 1121–1131.

Forstermann U., Munzel T. Endothelial Nitric Oxide Synthase in Vascular Disease: From Marvel to Menace. Circulation 2006; 113: 1708–1714.

Massion P. B., Feron O., Dessy C. et al. Nitric oxide and cardiac function: ten years after, and continuing. Circ Res. 2003; 93: 388–398.

Fischmann T. O., Hruza A., Niu X. D. et al. Structural characterization of nitric oxide synthase isoforms reveals striking active-site conservation. Nat. Struct. Biol. 1999; 6 (3): 233–42.

Volgina G.V. Contrast - induced nephropathy. Radiology - Practice 2007; 6: 42-53.

Tumlin J., Stacul F., Adam A. et al. Pathophisiology of contrast-induced nephropathy. Am.J.Cardiol. 2006; 98:14К-20К

Andrew S. Levey, Lesley A. Stevens, Christopher H. Schmid. et al. A New Equation to Estimate Glomerular Filtration Rate. Ann Intern Med. 2009 May 5; 150(9): 604–612.

Furchgott R.F., Zawadski J.V. The obligatory role of endothelial cells in relaxation of arterial smooth muscle by acetylcholine. Nature 1980; 288: 373– 376.

Reutov V.P. Biomedical aspects of nitric oxide and superoxide anionradical cycles. Vestn. Academy of Medical Sciences of Ukraine 2000; 3: 35–41.

Andrew P.J., Mayer B. Enzymatic function of nitric oxide synthases. Cardiovasc. Res. 1999. 43: 521–531

Chand S., Chue C.D., Edwards N.C. et al. Endothelial nitric oxide synthase single nucleotide polymorphism and left ventricular function in early chronic kidney disease. PLOS ONE 2015; 22(10): 1-10.

Ilhan N., Ates K., Ilhan N. et al. eNOS Glu298Asp Polymorphism and Endothelial Dysfunction in Patients with and without End-stage Renal Disease. Balkan Med J. 2016; 33(2): 128 - 37.

Marson B.P., Dickel S., Ishizawa M.H. et al. Endothelial nitric oxide genotypes and haplotypes are not associated with end-stage renal disease. DNA Cell Biol. 2011; 30(1): 55 - 9.

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Published
2020-02-28
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How to Cite
Sagynbaeva G. A., & Kaliev R. R. (2020). ROLE OF T-786C ENDOTHELIAL GENE POLYMORPHISM OF NO - SYNTHASE IN THE DEVELOPMENT OF ACUTE CONTRAST-INDUCED NEPHROPATHY IN PATIENTS WITH CORONARY HEART DISEASE. International Academy Journal Web of Scholar, (2(44), 64-71. https://doi.org/10.31435/rsglobal_wos/28022020/6921