Approximately 20 to 30 percent of patients with acute kidney injury (AKI) progress to chronic kidney disease (CKD). The mechanisms underlying this AKI-to-CKD transition mainly involve cellular damage, oxidative stress, mitochondrial dysfunction, and abnormal immune cell activation. Macrophages, as the primary immune effector cells infiltrating the kidney after AKI, exhibit high heterogeneity and plasticity in their phenotypes, mediating processes including renal injury, inflammation, repair, and fibrosis. Given the lack of specificity in broad-spectrum macrophage intervention strategies, which may disrupt protective macrophage subpopulations, it is imperative to develop therapeutic agents targeting pathogenic macrophage subsets in the kidney. Nanomedicines demonstrate advantages in treating kidney diseases by targeting pathogenic macrophages, leveraging their tunable physicochemical properties, superior biocompatibility, and biological barrier penetration capabilities. This article primarily introduced the phenotypic changes and functional heterogeneity of macrophages during the transition from AKI to CKD, the application methods of nanomedicines targeting renal macrophages, and the impact of the glomerular filtration barrier on the filtration of nanomedicines targeting renal macrophages.