The endothelium is a functional barrier composed of a single layer of endothelial cells between the vessel wall and circulating blood. The human vascular bed has a combined surface area of 1000 m2 and contains 1013 endothelial cells. The endothelium is the largest endocrine organ, with also important paracrine and autocrine functions (Perry & Pearson, 1989). Endothelial cells play important roles in haemostasis, vasoactivity, cellular proliferation, immunological reactions and inflammatory events. Therefore, endothelial dysfunction can lead to vasoconstriction, local ischemic phenomena and hypertension, thrombus formation and plaque growth and rupture, vascular proliferation and remodeling, and immunologic inflammation processes. Risk factors for endothelial dysfunction include old age, hypertension, diabetes mellitus, hypercholesterolemia, tobacco, menopause, male gender and obesity (Muller & Griesmacher, 2000; Raitakari & Celermajer, 2000). Cardiovascular disease is the leading cause of mortality in dialysis patients. In large crosssectional studies of dialysis patients, traditional cardiovascular risk factors such as hypertension and hypercholesterolemia have been found to have low predictive power, while markers of inflammation and malnutrition are highly correlated with cardiovascular mortality. However, the pathophysiology of the disease process that links uremia, inflammation, and malnutrition with increased cardiovascular complications is not well understood. In uremia, endothelial dysfunction derives from a systemic altered milieu that is partially aggravated by the dialysis treatment itself. From water quality to the type of membrane employed, many artificial factors intervene that trigger inflammatory processes culminating with endothelial damage, smooth muscle cell hyperplasia, fibrosis and vascular calcification. The underlying vascular disease consists mainly of two types, arteriosclerosis and atherosclerosis. Arteriosclerosis is mainly characterized by premature arterial aging with loss of elastic fibers and increased stiffness. Atherosclerosis is characterized by intima-media thickening, plaque formation and luminal narrowing. Both processes may interact simultaneously, possibly via diverse mechanisms, as endothelial dysfunction, shear stress, and elastic fiber fragmentation (Fishbein & Fishbein, 2009; Guerin et al., 2008; London & Drueke, 1997). Endothelial dysfunction is a well-documented early phenomenon in atherosclerosis that precedes structural changes and clinical manifestations, particularly in dialysis patients (Frick & Weidinger, 2007). Decreased endothelial function is thought to primarily reflect a decreased bioavailability of nitric oxide, a critical endothelium-derived vasoactive factor