Immune-mediated tubule atrophy promotes acute kidney injury to chronic kidney disease transition.
Ontology highlight
ABSTRACT: Incomplete repair after acute kidney injury can lead to development of chronic kidney disease. To define the mechanism of this response, we compared mice subjected to identical unilateral ischemia-reperfusion kidney injury with either contralateral nephrectomy (where tubule repair predominates) or contralateral kidney intact (where tubule atrophy predominates). By day 14, the kidneys undergoing atrophy had more macrophages with higher expression of chemokines, correlating with a second wave of proinflammatory neutrophil and T cell recruitment accompanied by increased expression of tubular injury genes and a decreased proportion of differentiated tubules. Depletion of neutrophils and T cells after day 5 reduced tubular cell loss and associated kidney atrophy. In kidney biopsies from patient
SUBMITTER: Xu L
PROVIDER: S-EPMC9391331 | biostudies-literature | 2022 Aug
REPOSITORIES: biostudies-literature
ACCESS DATA