Abstract
Acute kidney injury (AKI), a rapid loss of renal function, is a major clinical problem associated with a high degree of morbidity and mortality. During AKI, a stressor, such as ischemia-reperfusion (IR), causes tubular cell death, interstitial inflammation and vascular damage. Recovery from AKI depends on the ability of renal epithelial cells to repopulate denuded nephron segments. Surviving epithelial cells de-differentiate, migrate to the injury site, proliferate, and then re-differentiate to establish epithelial polarity and restore kidney function. Recovery from AKI, however, is less complete if the injury is severe or if organ damage preexists. This is particularly true in older individuals, in whom AKI is often followed by a disturbed repair process leading to a higher risk of permanent kidney damage.1
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