Clusterin marks maladaptive regenerative responses throughout the kidney following ischemia reperfusion.

Nevertheless, kidney tubules maintain a limited capacity to regenerate following various insults, through transient de-differentiation of the tubular epithelium into a progenitor phenotype. Recent studies describing the transcriptional changes underlying this process have primarily focused on proximal tubules with few studies examining the regenerative potential of other renal segments.

To address this knowledge gap, we employed single cell RNA sequencing (scRNAseq) and lineage tracing experiments to dissect the transcriptional changes in cells expressing the secreted factor Clusterin (Clu), a known biomarker and potential regulator of acute kidney injury (AKI) in mice and humans. Our data indicates that de novo induction of Clu mRNA serves initially as a robust marker of injured distal tubules and collecting duct cells following ischemia reperfusion injury (IRI).