The transition of AKI to CKD has major clinical significance. As reviewed here, recent studies
show that a subpopulation of dedifferentiated, proliferating tubules recovering from AKI
undergo pathologic growth arrest, fail to redifferentiate, and become atrophic. These
abnormal tubules exhibit persistent, unregulated, and progressively increasing profibrotic
signaling along multiple pathways. Paracrine products derived therefrom perturb normal
interactions between peritubular capillary endothelium and pericyte-like fibroblasts, leading …