Syndecan-1-mediated loading of VEGF-A into small extracellular vesicles facilitates peritubular capillary repair during AKI-to-CKD transition.

Acute kidney injury (AKI) is a severe clinical event with a high risk of transitioning to chronic kidney disease (CKD). Persistent hypoxia resulting from peritubular capillaries (PTCs) loss is a key factor driving this chronic transition. However, the mechanisms governing PTCs injury and repair, particularly under different AKI severity, remain unclear.

Kidney hepcidin protects the collecting duct against ferroptosis in ischemia/reperfusion-induced acute kidney injury.

Introduction: Ischemic acute kidney injury (AKI) frequently occurs in the intensive care unit. However, early diagnosis is challenging, and specific treatment strategies are still lacking. Here, our study identified endogenous hepcidin was induced with increasing severity of ischemia/reperfusion (I/R) injury mostly in collecting duct (CD) principal and intercalated cells.