[Alterations of the arterial vessel wall in renal failure].
Cardiovascular events are the main cause of death in patients with end-stage renal disease. Functional and structural alterations of the arterial system substantially contribute to the high cardiovascular mortality in these patients. Structural alterations of the arterial wall comprise intima-media thickening and atherosclerotic plaque formation. Moreover, mechanical vessel wall properties of large arteries are significantly disturbed. This is already observed in young patients. Reduced arterial distensibility impairs large artery cushioning function. This results in increased ventricular afterload promoting left ventricular hypertrophy and in reduced coronary perfusion. After renal transplantation, structural alterations of the arterial wall and disturbed mechanical vessel wall properties persist. Moreover, renal failure is characterized by a severe impairment of endothelial function. Disturbed endothelial function results from reduced production 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 structural lesions of the arterial wall. Also in renal transplant recipients, substantially impaired endothelial function is observed despite correction of uremia. Hyperparathyroidism commonly observed in renal failure contributes to the disturbed functional vessel wall properties of large arteries. In patients with end-stage renal disease, decreased large artery distensibility is an independent risk factor for increased cardiovascular mortality. This may apply also to intima-media thickening and to impaired endothelial function.
Hausberg
M
M
Medizinische Poliklinik, Westfälischen Wilhelms-Universität Münster. hausber@uni-muenster.de
Kisters
K
K
Kosch
M
M
Barenbrock
M
M
D001161:Arteriosclerosis / Q000209:etiology / Q000503:physiopathology*; D001808:Blood Vessels / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D006961:Hyperparathyroidism / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D051437:Renal Insufficiency / Q000150:complications / Q000503:physiopathology*; D017539:Tunica Intima / Q000503:physiopathology; D017540:Tunica Media / Q000503:physiopathology; D014511:Uremia / Q000209:etiology
D019001:Nitric Oxide Synthase
Gefässwandveränderungen bei Niereninsuffizienz.