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There is ample evidence showing that acute kidney injury (AKI) increases the risk of developing chronic kidney disease (CKD). Although considerable efforts have been undertaken in recent years to elucidate the mechanisms responsible for the AKI to CKD transition, many questions remain to be answered. In this review, we address most of the latest studies elucidating the mechanisms involved in this transition. Based on recent studies, the consensus to date is that endothelial and proximal tubular epithelium injury along with the activation of inflammatory processes occurring after an AKI episode, not only establish a close interrelation but also trigger a series of signaling pathways that culminate in the generation of tubulointerstitial fibrosis and chronic hypoxia, which lead to the progressive deterioration of functional tissue. These events highlight that the tubular epithelium does not appear to be the same after cell damage occurs. In this review, we present the advances aimed at elucidating the mechanisms that lead to a maladaptive response and how sex hormones seem to be involved in a positive or negative adaptive response. Elucidating and characterizing the mechanisms responsible for the AKI to CKD transition are an indispensable preliminary step that will help to identify the most important actors in this process.

Integrative View of the Mechanisms that Induce Acute Kidney Injury and its Transition to Chronic Kidney Disease