Our established murine model of bilateral ischemic AKI (BiAKI) results in a significant increase in serum IL-6, urine neutrophil gelatiniase-associated lipocalin (NGAL), collagen type 3 deposition, renal fibrosis, and α-smooth muscle actin activity, with a persistent decrease in the glomerular filtration rate (GFR) after injury [5]. Here, LCN2 is linked to renal fibrosis.