Collectively, these results confirm that, in the early phase of AKI, miR-423-5p is cargoed in circulation by small EVs bearing endothelial markers, while in the long term after renal IRI, circulating miR-423-5p is cargoed by non-caspase-3–dependent EVs, with an increased contribution of large EVs. This evidence concerns the gene CASP3 and acute kidney injury.