The prevention of restenosis after angioplasty. Accumulating evidence suggests that circulating endothelial progenitor cells incorporate into sites of endothelial denudation. The circulating EPCs reflect not only repair capacity but also the health of the endothelium. Clinical studies have shown that circulating EPC numbers are decreased and associated with vascular events in hemodialysis patients. However, limited data are available about the role of EPCs for venous intimal hyperplasia in hemodialysis patients. Accordingly, we conducted this prospective study to evaluate the impact of circulating EPC number and function on the outcome of vascular access. After the angioplasty procedure, all the participants of this study were prospectively followed for one year under the same protocol at respective hemodialysis centers. Medications of the participants were continued or adjusted according to their original indications but not for the maintenance of their vascular accesses. Follow-up surveillance included physical examination and dynamic venous pressure monitoring at each hemodialysis session, and transonic examination of access blood flow rate immediately after the intervention followed by monthly examinations. The referring nephrologists were blinded to the EPC levels of their patients. When abnormal clinical or hemodynamic parameters fulfilling the original referral criteria were detected, patients were referred for repeat fistulography and angioplasty as appropriate. Anatomic success was defined as less than 30% residual stenosis. Clinical success was defined as an improvement from baseline in clinical or hemodynamic parameters indicative of access dysfunction. Success of the procedure was defined as the combination of anatomic and clinical success. Target-lesion restenosis was defined as more than 50% diameter reduction of the original target lesion. Primary patency of vascular access was defined as time until the next intervention on the access of any kind; secondary patency of vascular access was defined as time from the intervention until surgical revision or abandonment of the access. Angioplasty is associated with mechanical vascular injury, followed by an intensive local inflammatory response, platelet activation, thrombus formation, and intimal hyperplasia. Endothelial disruption is considered to be the primary event in the initiation of restenosis after balloon angioplasty. Besides acting as a mechanical barrier protecting smooth cell migration, a functional endothelium modulates local hemostasis and thrombolysis, and VE-821 inquirer regulates smooth muscle cell proliferation. The importance of endothelial integrity has been demonstrated in animal studies, suggesting that a functionally intact endothelium is requisite for the inhibition of intimal hyperplasia. Accordingly, it is believed that faster re-endothelialization may inhibit the formation of intimal hyperplasia. The traditional paradigm of re-endothelialization is based on the proliferation and migration of pre-existing mature adjacent endothelial cells. Increasing evidence suggests that the injured endothelium is regenerated by circulating EPCs and that the levels of EPCs reflect vascular repair capacity.