Given that renal tubular toxicity is one of the key pathophysiological concepts of AKI following contrast media exposure, it stands to reason that RIPC may prevent contrast-related AKI via (TIMP-2) × (IGFBP7)-mediated temporary cell cycle arrest and increased resistance of the renal tubular epithelial cells to the toxic effect of contrast media at the time of exposure.28 This evidence concerns the gene IGFBP7 and acute kidney injury.