A reduced number of circulating EPCs independently predicts atherosclerotic disease progression and future cardiovascular events. Furthermore, previous reports have indicated reduced number and impaired function of EPCs in chronic renal insufficiency. However, there is currently little data about the association between circulating EPC levels and risk of CIN. To clarify this issue, we tested the hypothesis that decreased circulating EPC levels may be associated with increased risk of CIN and subsequent major cardiovascular events in patients undergoing cardiovascular interventional procedures. This is the first study to show that decreased circulating EPC level is associated with a greater risk of CIN in patients undergoing percutaneous interventional procedures. Furthermore, patients with decreased circulating EPC number as well as CIN have increased cardiovascular events after percutaneous coronary or peripheral interventions. These findings suggest that reduced circulating EPC levels, reflecting attenuated endothelial repair capacity, may contribute to atherosclerotic disease progression and increased risk of cardiovascular events in patients who have developed CIN after interventional procedures. Measurement of EPC levels might be useful for screening high CIN risk population before undergoing percutaneous interventions. CIN, characterized by the development of acute renal failure after exposure to radiocontrast agents, is a common cause of hospital-acquired acute renal injury. Although CIN is generally benign in most PD325901 instances, it is associated with extended length of hospital stays, increased health care costs, and higher risk of death. As well as an increased risk of death, contrast-induced acute kidney injury is also associated with other adverse outcomes including late cardiovascular events after percutaneous interventions. The risk factors that may predispose patients to CIN after cardiovascular interventional procedures include advanced age, diabetes mellitus, dehydration, and pre-existing renal disease. Several strategies, including volume expansion, using iso-osmolar contrast, and limiting the amount of administered contrast media, have become well established methods for prevention of CIN. Although the exact mechanisms of CIN have yet to be fully elucidated, several causes have been described. Most likely, a combination of various mechanisms is responsible for the development of CIN. A reduction in renal perfusion caused by a direct effect of contrast media on the kidney, and toxic effects on the tubular cells are generally accepted as the main factors in the pathophysiology of CIN. Accumulating evidence suggests that the acute renal failure caused by the radiocontrast agents seems to be a consequence of an imbalance between vasoconstrictor factors and vasodilator agents like the prostaglandins or NO. The role of NO in renal hemodynamics regulation has been reported in many studies. A decreased NO synthesis, or a lack of response of the endothelium to vasodilators, have been suggested as possible mechanisms for the ischemic or the nephrotoxic ARF.