Endothelial dysfunction is central to the pathophysiology of vascular ischemia, bacterial sepsis, toxin-induced thrombotic microangiopathy, and antibody-mediated kidney transplant rejection and often manifest with renal failure. With each of these diagnoses circulating components of the complement cascade bind to endothelial cells and induce disease progression through anaphylactic cellular messaging, monocyte homing, and direct cell membrane disruption. In response to injury during embryologic development avascular metanephric blastema initiate endothelial differentiation. Although circulating hematopoietic progenitor cells have shown therapeutic promise they incorporate into renal vasculature at very low density.
