Abstract
Acute kidney injury (AKI) is common, and depending on the severity and frequency of the insult, can contribute to the development of chronic kidney disease (CKD).1 Although the cellular and molecular mechanisms necessary for the restoration of kidney function after AKI remain to be elucidated, failed differentiation and maladaptive repair are now recognized as important contributors to the AKI-to-CKD transition. Several mechanisms are thought to be involved in this transition: fibrosis due to capillary rarefaction and tissue hypoxia, the infiltration of inflammatory cells that contribute to the repair process after AKI, and cell cycle arrest during AKI.
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