Decreased Number and Impaired Angiogenic Function of Endothelial Progenitor Cells in Patients With Chronic Renal Failure

Abstract

Objective— Increased risk of cardiovascular disease in patients with chronic renal failure (CRF) has been explained by accelerated atherosclerosis and impaired angiogenesis, in which endothelial progenitor cells (EPCs) may play key roles. We hypothesized that altered EPC biology may contribute to the pathophysiology of CRF. Methods and Results— EPCs were isolated from CRF patients on maintenance hemodialysis (n=44) and from a normal control group (n=30). CRF patients showed markedly decreased numbers of EPC (44.6%) and colonies (75.3%) when compared with the controls (P<0.001). These findings were corroborated by 30.5% decrease in EPC migratory function in response to vascular endothelial growth factor (VEGF) (P=0.040) and 48.8% decrease in EPC incorporation into human umbilical vein endothelial cells (HUVEC) (P<0.001). In addition, Framingham’s risk factor score of both CRF (r=−0.461, P=0.010) and normal group (r=−0.367, P=0.016) significantly correlated with the numbers of EPC. Indeed, the number of cir... Our study shows that EPC is numerically and functionally impaired in CRF. This may contribute to the accelerated atherosclerosis and impaired angiogenesis observed in patients with CRF. Altered biology of EPC may therefore account for the increased cardiovascular disease risk in CRF.