Patients with chronic renal failure have an increased risk of cardiovascular disease. This has been explained by accelerated atherosclerosis and impaired angiogenesis, in which endothelial progenitor cells (EPCs) play key roles. This study hypothesized that altered EPC biology may contribute to the pathophysiology of chronic renal failure.
This study notes that EPC biology, which is critical for neovascularization and the maintenance of vascular function, is altered in cases of chronic renal failure. The data strongly suggest that the dysfunction of circulating EPC has a role in the progression of cardiovascular disease in patients with chronic renal failure.
