Acute kidney injury (AKI) is a common disease characterized by a sharp decline of kidney function within a short time and is associated with high morbidity and mortality in recent years. Although the development of clinical therapy for AKI has taken a certain degree of effect, these treatments do little to improve the prognosis of patients suffering from AKI. Mounting researches have demonstrated that AKI is an independent and important risk factor for chronic kidney disease (CKD), and the transition from AKI to CKD involves various mechanisms. Recently, in addition to the pathophysiology of tubular epithelial cells (TECs) and macrophages aberrant polarization, the crosstalk between them has garnered significant attention after kidney injury. The crosstalk between TECs and macrophages polarization is closely related to inflammation, repair and fibrosis after kidney injury, which are all key points in the transition from AKI to CKD. Exploring the progression of AKI to CKD is of great significance for clinical treatment. Therefore, this review aims to summarize the current researches on tubular epithelial cells, macrophages and the crosstalk them to provide effective reference for subsequent research and help to find potential therapeutic targets to prevent the progression of AKI to CKD.