Several experimental and clinical studies showed that increased oxidative stress in dialysis patients may be due to inhibition of nitric oxide (NO) synthesis by ADMA (Asymmetric Dimethylarginine ), known to be endogenous inhibitor of NO synthetase [15]. ADMA may be significantly reduced by dialysis [16]. Metabolism of ADMA is primarily by the enzyme DDAH , which activity is decreased by inflammation, oxidative stress, diabetes mellitus and hypercholesterolemia [17 ]. It was proposed that circulating ADMA may be one mechanism accounting for the resistant hypertension and overfluid in dialysis patients [17 ].