Injury, repair, and resolution during ischemic acute kidney injury (AKI). Following ischemia, there is substantial microvascular injury, leading to increased coagulation, reduced nitric oxide release, macrophage recruitment, and increased hypoxia. These events in turn lead to significant tubular injury and death, ultimately causing a decrease in glomerular filtration rate (GFR). Following reperfusion, the kidney enters adaptive repair in which inflammation and debris begins to resolve through a switch from M1 macrophages to M2 macrophages. Both endothelial repair and epithelial tubular proliferation begin, leading to resolution. Adapted from Fernenback and Bonventre [121] with permission from Macmillan Publishers Ltd