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Role of high-density lipoprotein cholesterol in renovascular disease treatment.

Ischemic renal or renovascular disease is a reduction in glomerular filtration rate (GFR) and loss of renal parenchyma, caused by renal artery stenosis. Ischemic renal disease presents itself in the setting of extrarenal arteriosclerotic vascular disease, endothelial dysfunction, and also azotemia in older patients. Atherosclerotic renal artery disease is common in individuals with coronary artery disease and aortic and peripheral vascular disease. 1 Risk factors for ischemic nephropathy are the same as those for coronary artery disease, so it seems that patients with renovascular disease die because of cardiovascular complications more than the progress to end-stage renal disease. 2 In patients with atherosclerosis, the initiator of endothelial injury is not clear but hypertension, dyslipidemia, diabetes mellitus, cigarette smoking, viral infection, immune injury, and increased homocysteine levels may contribute to endothelial injury. Endothelial dysfunction is implicated in lesion creation by the support of both the early and late mechanisms of atherosclerosis including up-regulation of adhesion molecules, increasing chemokine secretion, leukocyte adherence and cell permeability, enhanced low-density lipoprotein cholesterol oxidation, platelet activation, and vascular smooth muscle cell proliferation and migration. Nitric oxide production is diminished, and an imbalance in the role of endothelium-derived relaxing factor and contracting factor would appear, corresponding to the endothelium actions moved toward reduced vasodilation, a proinflammatory state with prothrombic properties. 3-5