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 circulating EPC was significantly lower in CRF patients than in normal group under the same burden of risk factors (P <0.001). A significant correlation was also observed between dialysis dose (Kt/V) and EPC incorporation into HUVEC (r =0.427, P =0.004).Conclusions—
EPC biology, which is critical for neovascularization and the maintenance of vascular function, is altered in CRF. Our data strongly suggest that dysfunction of circulating EPC has a role in the progression of cardiovascular disease in patients with CRF.