#3145 ASSOCIATION OF ENDOTHELIAL NITRIC OXIDE SYNTHASE GENE POLYMORPHISM WITH ENDOTHELIAL DYSFUNCTION IN DIABETIC NEPHROPATHY AMONG AZERBAIJANIS

Abstract Background and Aims Vascular endothelial dysfunction resulting from impaired nitric oxide synthase (NOS) activity in the cells of blood vessels has been suggested as playing an important role pathogenesis Diabetic nephropathy (DN). It regulates function maintains endothelial-dependent vasodilation multiple organs, including kidney. The study was carried out to investigate association T-786C single nucleotide polymorphisms with flow mediated dilation (FMD) DN among type 2 diabetic subjects. Method 90 patients (45 male 45 female) were recruited Nephrology Endocrinology departments Azerbaijan Medical University hospital. As a control group results compared findings 100 healthy Azerbaijani individuals (50 males 50 females). approved by ethics committee informed consent obtained all written form. Brachial determined brachial artery vasodilator response or FMD dominant arm according previously validated techniques. T786C polymorphism detected using polymerase chain reaction-restriction fragment length analysis. Results showed significant differences between regarding genotype allele distributions polymorphisms. CC significantly more frequent diabetics than (42% vs. 8%, p = 0.01). homozygote T786C(TT), T786C(CC) heterozygote T786C(CT) respectively 13.5 ±0.16%, 12.3±0.19%,13.9 ±0,28%. In groups, dominance C mutant homozygous gene eNOS. Subjects 786C(CC) (n 48) reduced those (TT) 7) (p 0.021) (CT) 35) 0.023), whereas there no difference endothelial-independent these groups. Although subjects did not show levels FMD. Who carriers demonstrated markedly noncarriers 0.019). Conclusion data suggest that nephropathy, eNOS may be involved dysfunction.