TIMP2 and acute kidney injury: 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