Figure 3 Pathophysiological events and preventive

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Figure 3 Pathophysiological events and preventive strategies in contrast-induced acute kidney injury (CIAKI) Figure 3 | Pathophysiological events and preventive strategies in contrast-induced acute kidney injury (CIAKI). Contrast agents damage several components of the kidney (blue boxes). Contrast medium toxicity induces membrane damage in epithelial and endothelial cells. Endothelial dysfunction and vasoactive substances released from epithelial cells cause vasoconstriction. Afferent arteriolar constriction results in a rapid decrease in glomerular filtration rate (GFR)67. The outer medulla is at risk of CIAKI owing to its high metabolic demand and comparatively low perfusion via the vasa recta74. The latter constricts when exposed to contrast medium59. Concomitant cell damage takes place owing to hypoxia, initiating apoptosis and aggravating renal hypoperfusion by cell oedema and further vasoconstriction. Concentration of contrast medium in the tubules and vasa recta increases fluid viscosity, which compromises urine and blood flow84, thus decreasing GFR and oxygenation, and prolonging contrast medium exposure. Strategies for prevention of CIAKI such as fluid expansion and decreasing oxidative stress are based on pathophysiological knowledge (green boxes). NO, nitric oxide. Fähling, M. et al. (2017) Understanding and preventing contrast-induced acute kidney injury Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.196