M1/M2 macrophage balance depending on chronic kidney disease (CKD) progression. Renal function varies over time, depending on the type of injury, the persistence and severity of the damage and the reparative ability of the kidney. In the early stages of CKD, pro-inflammatory macrophages (M1) infiltrate the injury site and release pro-inflammatory cytokines, which promote an inflammatory state. If the injury resolves, renal function as well as renal mass ameliorate, depending on damage severity and duration. Macrophages also switch to an anti-inflammatory (M2) phenotype, leading to a wound healing phase that may involve tissue fibrosis. However, if there is no injury resolution, M1 macrophages persist at injured sites and there is a decrease in the number of M2 macrophages, which could also subsequently undergo a phenotypic switch to M1. The continuous release of profibrotic and inflammatory factors promote renal fibrosis, leading to renal failure.