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]. This evidence concerns the gene FABP1 and acute kidney injury.