Abstract
Acute kidney injury (AKI), triggered by ischemia, sepsis, toxicity, or obstruction, is marked by a rapid impairment of renal function and could lead to the initiation and advancement of chronic kidney disease (CKD). The concept of AKI to CKD transition has gained much interest. Despite a series of studies highlighting the diverse roles of renal macrophages in the immune response following AKI, the intricate mechanisms of macrophage-driven cell-cell communication in AKI to CKD transition remains incompletely understood. In this review, we introduce the dynamic phenotype change of macrophages under the different stages of kidney injury. Importantly, we present novel perspectives on the extensive interaction of renal macrophages with adjacent cells, including tubular epithelial cells, vascular endothelial cells, fibroblasts, and other immune cells via soluble factors, extracellular vesicles, and direct contact, to facilitate the transition from AKI to CKD. Additionally, we summarize the potential therapeutic strategies based on the adverse macrophage-neighboring cell crosstalk.