These AKI biomarkers can be classified into tubular damage biomarkers (mainly filtered urinary proteins normally reabsorbed by intact proximal tubular cells, such as beta-2 microglobulin or N-acetyl-beta-d-glucosaminidase), biomarkers whose genes are induced or downregulated by AKI (neutrophil gelatinase associated lipocalin (NGAL), interleukin-18 (IL-18) and kidney injury molecule-1 (KIM-1), for example) or biomarkers of cell cycle arrest (tissue inhibitor of metalloproteinases-2 (TIMP-2) and insulin-like growth factor binding protein-7 (IGFBP-7), for example) [7]. This evidence concerns the gene IGFBP7 and acute kidney injury.