Acute kidney injury (AKI) dramatically increases mortality of hospitalized patients. Incidences have been increased in recent years. The most frequent cause is transient renal hypoperfusion or ischemia which induces significant tubular cell dyfunction / damage. In addition, two further events take place: interstitial inflammation and microvasculopathy (MV). The latter evolves within minutes to hours post-ischemia and may results in permanent deterioration of the peritubular capillary network, ultimately increasing the risk for chronic kidney disease (CKD) in the long-term. In recent years, our understanding of the molecular / cellular processes responsible for acute and sustained microvasculopathy has increasingly been expanded. The methodical approaches for visualizing impaired peritubular blood-flow and increased vascular permeability have been optimized, even allowing to depict tissue abnormalities in a three-dimensional manner. In addition, endothelial dysfunction, a hallmark of MV is increasingly been recognized as inductor of both, vascular malfunction and interstitial inflammation. In this regard, so-called regulated necrosis of the endothelium could potentially play a role in postischemic inflammation. Endothelial Progenitor Cells, represented by at least two major subpopulations have been shown to promote vascular repair in experimental AKI, not only in the short- but also in the long-term. The discussion about the true biology of the cells continues. It has been proposed that early EPCs are most likely myelomonocytic in nature, thus they may simply termed as proangiogenic cells (PACs). Nevertheless, the reliably protect certain types of tissues / organs from ischemia-induced damage, mostly by modulating the perivascular microenvironment in a direct manner. Aim of the current article is to summarize the current knowledge on postischemic MV and EPC-mediated renal repair.