Figure 14. A potential role for vascular dropout in promoting the development of CKD following AKI.

Acute injury has the potential to affect both tubular and vascular compartments. In addition to direct injury to the microvascular compartment, tubular injury may compromise normal vascular support, shifting the environment to one which promotes vascular impairment rather than vascular stability, including the loss of VEGF expression, the increase in TGF-beta expression as well as several other angio inhibitory compounds. The resultant decrease in capillary structures has a number of potential consquences on renal function including the exacerbation of hypoxia and the impairment of Na handling hemodynamic responses. Hypoxia, along with the potential endothelial mesenchymal transition are likely to participate in the development of fibrosis, which is also influenced by sustained immune/ inflammatory activity. The figure modified from and earlier version published in citation (29).