Abstract

The leading cause of high mortality in dialyzed patients is cardiovascular disease. One of the main contributors of cardiovascular event is vascular calcification, which occurs even in very young patients. Multiple factors and complex mechanisms are involved in the formation of robust vascular calcification which affects a large vascular area observed in chronic kidney diseases. Patients on dialysis are exposed to enhanced oxidative stress as a result of increased pro-oxidant activity and reduced anti-oxidant systems. The oxidation of lipoprotein particles is implicated in the development of vascular damage representing oxidative threat, which leads to endothelial dysfunction. Moreover, in a pro-oxidant environment osteoblastic trans-differentiation of smooth muscle cells was shown to occur. Heme derived from oxidized hemoglobin might contribute to the formation of reactive lipid metabolites. This oxidative burden contributes to the development of atherosclerosis and vascular calcification. Heme oxygenase-1 and ferritin may serve as intracellular defense mechanisms against such an insult.

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