Alterations of the arterial wall in renal failure

Cardiovascular events are the main cause of death in patients with end-stag e renal disease. Functional and structural alterations of the arterial syst em substantially contribute to the hi,oh cardiovascular mortality in these patients. Structural alterations of the arterial wall comprise intima-media thickening and atherosclerotic plaque formation. Moreover, mechanical vess el wall properties of large arteries are significantly disturbed. This is a lready observed in young patients. Reduced arterial distensibility impairs large artery cushioning function. This results in increased ventricular aft erload promoting left ventricular hypertrophy and in reduced coronary perfu sion. After renal transplantation, structural alterations of the arterial w all and disturbed mechanical vessel wall properties persist. Moreover, renal failure is characterized by a severe impairment of endothel ial function. Disturbed endothelial function results from reduced productio n of endothelium-dependent endogenous vasodilators and/or blunted vascular effects of these substances. Uremia is associated with the accumulation of an endogenous inhibitor of the endothelial nitric oxide synthase. Impaired endothelial function in renal failure promotes the progression of structura l lesions of the arterial wall. Also in renal transplant recipients, substa ntially impaired endothelial function is observed despite correction of ure mia. Hyperparathyroidism commonly observed in renal failure contributes to the d isturbed functional vessel wall properties of large arteries. In patients with end-stage renal disease, decreased large artery distensibi lity is an independent risk factor for increased cardiovascular mortality. This may apply also to intima-media thickening and to impaired endothelial function.