Acute kidney injury (AKI) is a widespread health problem, with increased incidence among hospitalized patients. The most common cause of AKI is ischemic injury, which targets the proximal tubule causing damage to kidney structure and function. Within ischemic AKI, overactivation of the renin angiotensin system (RAS) can drive pathologic changes. Angiotensin converting enzyme 2 (ACE2) is an integral part of the RAS and is highly expressed along the brush border of the proximal tubule (PT), where it acts to enzymatically degrade angiotensin II (AngII) and extinguish its effects. While several studies have examined the protective role ACE2 plays within chronic kidney disease and hypertension, less is known about ACE2 in acute injury. Here, we hypothesize that ACE2 overexpression is protective against AKI through local AngII metabolism and promotes recovery of renal function after AKI.