Tubule atrophy and fibrosis often develop after acute kidney injury (AKI) favoring transition to chronic kidney disease (CKD). The AKI-CKD transition has major implications, but poorly understood. We found that tubules regenerating after AKI often fail to differentiate. Such tubules are growth arrested and atrophic, and exhibit signaling that drives fibrosis. The cause of this pathology is unknown. We obtained three lines of evidence that could explain why recovering tubules become atrophic and profibrotic.
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