Non-traditional cardiovascular disease risk factors in end-stage renal disease: oxidate stress and hyperhomocysteinemia

Studies in experimental animals have shown that oxidative stress and hyperhomocyst(e)inemia culminate in abnormal vascular and endothelial regulation, functional nitric oxide deficiency, vascular hypertrophy, and atherosclerosis. Oxidative stress is accompanied by increased advanced glycation endproducts and oxidized low density lipoproteins. Studies of patients with end-stage renal disease provide extensive indirect, evidence of increased oxidative stress and more than ninety percent are hyperhomocyt(e)inemic. Presently, only uncontrolled or observational studies are available to assess the effects of anti-oxidant therapy for oxidative stress or folate therapy for hyperhomocyst(e)inemia in these patients. Promising developments include the reports of beneficial effects of a vitamin E coated dialyzer, and the reduction in homocyst(e)ine levels in patients with end-stage renal disease given an intravenous folate metabolite. However, there is presently no therapy available to reverse fully oxidative stress or hyperhomocyst(e)inemia. Therefore, the causative role of these nontraditional risk factors of cardiovascular disease remains untested.