associated with endothelial dysfunction, cannot fully account for the advanced state of arterial stiffening and the high rate of cardiovascular morbidity and mortality. 23 However, accumulation of naturally occurring nitric oxide synthase (NOS) inhibitors may offer a potential explanation. Plasma concentration of asymmetrical dimethylarginine (ADMA), a potent endogenous competitive inhibitor of NOS, can reach levels of 7.5-times normal in patients with ESRD. 24 Endothelial dysfunction in uremic children is related to plasma ADMA levels. 25 More recently, ADMA was noted to be an independent predictor of total and cardiovascular mortality, and of the severity of carotid atherosclerosis in hemodialysis patients. 26 Multivariate analysis showed that a 2-μmol/L increase in plasma ADMA (an almost doubling of normal values) was associated with a 37% increase in risk for fatal and nonfatal cardiovascular events. Thus, ADMA may represent an independent risk factor in ESRD, leading to further reduction in NO, endothelial dysfunction, arterial stiffening, and predisposition to increased cardiovascular events.