It remains a clinical dilemma to directly evaluate the etiologies of AKI without resorting to renal biopsy despite numerous biomarkers having been proposed within recent decades as indicators for the specific site of nephron damage, including neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, liver-type fatty acid-binding protein (L-FABP), kidney injury molecule-1 (KIM-1), and interleukin 18 (IL-18), among others [14,15]. This evidence concerns the gene LCN2 and acute kidney injury.