Abstract: Acute kidney injury (AKI) is an important risk factor for the occurrence and development of chronic kidney disease(CKD). Even milder AKI could have adverse consequences and could progress to renal fibrosis, which is the ultimate common pathway for terminal kidney diseases. Therefore, it is crucial to gain an indepth understanding of the mechanism to block the transition from AKI to CKD. This article reviews the cellular and molecular mechanisms of the transition from AKI to CKD and the research progress of potential therapeutic targets.

Key words: acute kidney injury, chronic kidney disease, renal tubular epithelial cells, fibroblasts, tertiary lymphoid tissue