In recent years, authors have found the presence of renal tubular injury to be the mechanism underlying the development of AKI, as determined based on the levels of urinary biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL), liver fatty acid-binding protein (LFABP) and N acetyl-β-D glucosaminidase (NAG), in patients with contrast media-induced nephropathy or a history of cardiac surgery and those receiving intensive care [6–11]. Here, LCN2 is linked to acute kidney injury.