INSIGHTS INTO ACUTE KIDNEY INJURY AND TRANSITION TO CHRONIC KIDNEY DISEASE BY SINGLE-CELL TECHNOLOGIES.

Abstract

Outcomes after acute kidney injury (AKI) cover a wide spectrum ranging from full recovery to incomplete repair leading to transition to chronic kidney disease (CKD). This "AKI to CKD transition" is incompletely understood at a cellular level and there is a pressing need to identify the basic mechanisms of successful recovery from AKI and to develop therapeutic interventions to prevent the AKI to CKD transition. In recent years, single-cell transcriptomic and epigenomic technologies have substantially improved our understanding of cell types and states in homeostasis and after injury. In this paper, I will review our recent work applying single-cell technologies to better understand AKI and its transition to CKD, focusing on a proximal tubule cell state that we have termed "failed repair." Failed repair proximal tubule cells are characterized by pro-inflammatory and pro-fibrotic gene expression patterns and may drive the AKI to CKD transition.