Vascular progenitor cells show promise for the treatment of microvasculature endothelial injury. We investigated the function of renal artery progenitor cells derived from radical nephrectomy patients, in the setting of acute ischemic and hyperperfusion injuries. Present in adventitia, CD34positive/CD105negative cells were clonal and expressed transcription factors Sox2/Oct4 as well as surface markers CXCR4 (CD184)/KDR(CD309) consistent with endothelial progenitor cells. Termed renal artery-derived vascular progenitor cells (RAPC), these cells localized to the kidney after kidney-specific injury, where they integrated with the renal microvasculature in two animal models including ischemia/reperfusion injury (IRI) and hyperperfusion injury. RAPC decreased serum creatinine after ischemia/reperfusion, reduced albuminuria after hyperperfusion, and increased renal perfusion in both models. At a cellular level, RAPC reduced endothelial injury in co-culture and promoted local endothelial migration. microRNA profiling identified high levels of miRNA 218 in RAPC. When transfected with LNA-mir218, RAPC demonstrated an increased rate of local migration in vitro. After IRI, injected RAPC transfected with LNA-mir218 were found in greater density in renal cells compared to RAPC transfected with scrambled LNA. In conclusion, RAPC reside in renal artery adventitia, localize to injured renal endothelium after intravenous injection, and promote renal microcapillary network repair. Our work shows the feasibility of pre-emptive progenitor cell procurement from a targeted patient population and potential future therapeutic use in the form of autologous cell transplantation.