Microvasculopathy in ischemic acute kidney injury: consequences and therapeutic implications.

Ischemic acute kidney injury (iAKI) is the most frequent type of hospital-aquired acute renal failure (ARF). Mortality of ARF still ranges between 30% and 50%. Although acute renal ischemia significantly affects function and structure of the tubular epithelium, postischemic interstitial inflammation and microvasculopathy both contribute to ongoing renal dysfunction. The renal vasculature shows a highly specialized architecture. Renal ischemia induces severe alterations of the endothelium in small peritubular arterioles and capillaries. Investigations performed in recent years point towards a new therapeutic approach in iAKI, that is to target postischemic endothelial dysfunction by administering cells of the endothelial lineage. With regard to endothelial-type cells, new perspectives are offered with the identificaton of endothelial progenitor cells (EPCs). Although heterogenous in nature, EPCs can be employed for anti-ischemic treatment in different situations. Meanwhile the cells have been shown to protect mice from iAKI and several strategies have been established in order to increase the renoprotective capacity of EPCs. Further investigations will help to clarify whether EPCs not only protect the kidney in the short- but also in the long-term.