Epithelial-Immune-Stromal Interactions Define Divergent Repair and Fibrosis Pathways After Acute Kidney Injury in Human Renal Transplants.

ABSTRACT: Acute kidney injury (AKI) is a major cause of early graft dysfunction after kidney transplantation, particularly in recipients of high-risk donor kidneys prone to ischemia-reperfusion injury. However, the cellular mechanisms dictating whether injury resolves or progresses to fibrosis remain unclear. This study combines single-nucleus RNA sequencing and imaging mass cytometry (IMC) analysis of human kidney allograft biopsies collected within eight weeks posttransplant, stratified by long-term functional outcomes. Grafts that recovered function were enriched in regenerative proximal tubular (PT) cells co-expressing PROM1, CD24, and injury markers, consistent with scattered tubular cells (STCs). In contrast, non-recovering grafts contained a unique subpopulation of transitional proxima

SUBMITTER: Azim S 

PROVIDER: S-EPMC12073942 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature