Driving role of macrophages in transition from acute kidney injury to chronic kidney disease

Acute kidney injury (AKI), characterized by acute renal dysfunction, is an increasingly common clinical problem and an important risk factor in the subsequent development of chronic kidney disease (CKD). Regardless of the initial insults, the progression of CKD after AKI involves multiple types of cells, including renal resident cells and immune cells such as macrophages. Recently, the involvements of macrophages in AKI-to-CKD transition have garnered significant attention. Furthermore, substantial progress has also been made in elucidating the pathophysiological functions of macrophages from the acute kidney to repair or fibrosis. In this review, we highlight current knowledge regarding the roles and mechanisms of macrophage activation and phenotypic polarization, and transdifferentiation in the development of AKI-to-CKD transition. In addition, the potential of macrophage-based therapy for preventing AKI-to-CKD transition is also discussed.

Automated summary

Acute kidney injury (AKI) is a common renal disorder and an important risk factor for the development of chronic kidney disease (CKD). Macrophages have been shown to play a crucial role in the transition from AKI to CKD, and significant progress has been made in understanding their pathophysiological functions. This review highlights the roles and mechanisms of macrophage activation, phenotypic polarization, and transdifferentiation in the development of AKI-to-CKD transition, and discusses the potential of macrophage-based therapy for preventing this transition.