Convincing evidence suggests that atherosclerosis is associated with endothelial dysfunction at the early stage of the disease process. Intact endothelium and maintenance of endothelial integrity play a pivotal role in preventing the development of atherosclerotic vascular disease. Recent insight suggests that the injured endothelial monolayer is regenerated by bone marrowderived EPC, and circulating EPCs correlate with important clinical outcomes in vascular health. They contribute to angiogenesis and organ repair in both animal and human models of ischemic injury. With regard to renal injury, they appear to home in on, and incorporate into sites of active neovascularization in the kidney. Pastchan et al. have demonstrated that, in mice models, renal ischemia rapidly mobilizes EPCs, which transiently home in on the spleen and subsequently accumulate in the medullopapillary region of the kidney. They also proved that EPC-enriched cells from the medullopapillary parenchyma afforded partial renoprotection after renal ischemia, implying an important role of the recruited EPCs in the functional rescue of renal ischemia. It appears that bone marrow-derived EPCs may play a critical role in improving kidney function after ischemic or nephrotoxic injury in experimental models. EPCs represent a very minor cell population in whole blood, and the choice of markers and controls is very important. However, there is still confusion about the definition used for EPC, and the circulating putative EPC identified in this study may include a monocyte subpopulation that may well have proangiogenic properties. However, in attempting an identification of EPC, a major limiting factor is that no simple definition of EPC exists at the present time, while various methods to define EPC have been reported. Therefore, we used CD34+, CD34+ KDR+, CD34+ KDR+ CD133+ markers to identify circulating EPCs in the current study. Our data showed reduced circulating EPC levels were associated with development of CIN, and subsequent cardiovascular events after percutaneous interventions. Recent evidence indicates that Tasocitinib mobilization and differentiation of EPCs are modified by NO, and that bone marrow-expressed eNOS is essential for the mobilization of stem cells and progenitor cells in vivo. Therefore, decreased NO concentrations in CIN patients may modulate EPC behaviors and result in impaired vascular repair capacity, which suggests a pivotal role of EPC in modulation of CIN, and that a reduced number of these cells gives rise to the poor prognosis in CIN patients. These findings further provide pathophysiological insights into CIN development and raise the possibility that circulating EPCs may be a target for preventive interventions in selected individuals. Some limitations of this study should be addressed. First, the sample size of this study was relatively small and may limit the interpretation of the study result. Due to the limited number of CIN patients, we were only able to adjust for 2 covariates in multivariate analysis to avoid over-fitting the problem.