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Considerable progress has been made in the treatment of end-stage renal disease over the past 20 yr. Nonetheless, the dialysis population continues to carry an excess mortality from fatal cardiovascular events [Baylis et al., 2006]. One possible explanation derives from the association of uremia and accelerated atherosclerosis [Tripathi et al., 2008]. The latter may be related to pre-dialysis factors such as preceding arterial hypertension, glucose intolerance, secondary hyperparathyroidism, dyslipidemia, and others. However, dialysis itself may further contribute to atherosclerosis by oxidative stress, cytokine stimulation, and other events inherent to hemodialysis (HD). Endothelial dysfunction has been shown recently to be a major initiating factor in atherosclerosis [Kone et al., 1997]. Endothelial dysfunction is associated primarily with decreased nitric oxide (NO). However, endothelial dysfunction of uremia has received little attention. Among the various factors involved in the deterioration of renal function, changes in the hemodynamic are thought to be important. Nitric oxide (NO), an important endothelium derived relaxing factor, is synthesized in the vascular endothelium by the NO synthase. NO is a potent regulator of intrarenal hemodynamics [Baylis et al., 2006 and Tolins et al., 1990]. At the release site it mediates local vasodilatation, antagonizes platelet aggregation, inhibits vascular smooth muscle cell proliferation and also, regulates some vessel-platelet interactions, limits the oxidation of atherogenic low density lipoproteins and has a vasoprotective effect by scavenging superoxide radicals and suppresses leukocyte adhesion to endothelial vessel wall. Multiple lines of evidence have suggested that NO plays a protective role in various important events during atherogenesis. Reduced NO levels are involved in the pathogenesis of the vascular endothelium due to the loss of its vasodilatory effect [Schmidt et al., 1994]. In the kidney, NO dilates renal blood vessels and modulates renin secretion [Kone et al., 1997 and Tripathi et al., 2008]. An impairment of NO production

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Plasma Total Nitric Oxide and Endothelial Constitutive Nitric Oxide Synthase (ecNOS) Inron 4 Gene Polymorphism: A Study in Children with Chronic Kidney Disease