LCN2 and acute kidney injury: Markers of inflammation (interleukin-18, matrix metalloproteinase-2), glomerular filtration rate (cystatin C), proximal tubular response [urinary liver-type fatty acid binding protein (L-FABP) kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL)], and tubular enzymes [N-acetyl-β-D glucosaminidase (NAG)] in serum and/or urine have all emerged as predictors of AKI before renal function decline can be detected clinically (12, , , –19).