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      • Poster Session : PS 0475 ; Nephrology ; 1PRMT-1 Gene Polymorphism in Hemodialysis Patients with Increased Adma Level

        ( Mochamad Yusuf ),( Mochamad Thaha ),( Nilamsari Wenny ),( Mochamad Amin ),( Dokter Pranawa ),( Yasuhiko Tomino ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1

        Background: A symmetric dimethylarginine (ADMA) is a potent endogenous inhibitor of nitric oxide synthases (NOS) which could reduce nitric oxide (NO) level and causesendothelial dysfunction, vasoconstriction, elevation of blood pressure, and as a potent predictor of cardiovascular event in end-stage kidney disease (ESKD) patients as well. Experimental evidence has convincingly shown that inhibition of NOS by ADMA leads to enhanced norepinephrine release from sympathetic nerves in rats and humans, whereas sympathetic activation impairs endothelium-dependent, nitric-oxide-mediated vasodilatation in healthy humans and ESKD patients. ADMA is formed through the catalytic activity of protein arginine methyltransferases (PRMTs). Thus, type 1 PRMT (PRMT-1) catalyzes the asymmetric dimethylation of arginine residues. Moreover, there are several pathways lead to the increased ADMA level, where PRMT-1 gene polymorphism has been one of the hypothesis. Methods: A total of 56 patients (total sampling) from a private hospital were enrolled in this study. Venous blood samples were taken just before hemodialysis. ADMA was measured using an enzyme-linked immuno- sorbent assay. All samples went through processes of DNA extraction, Polymerase Chain Reaction, and Electrophoresis. Thirteen out of 56 samples (consecutive) were further undergone DNA isolation and purifi cation, labelling, precipitation and sequencing. Genotyping of the polymorphisms was performed using PCR-based SNP detection methods (Applied Bio- systems, Carlsbad, USA)Conclusions: It appears that PRMT-1 gene polymorphism may partially explain the ADMA increasement in hemodialysis patients.

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