Editorial: contrast-induced acute kidney injury: shifting from elective to urgent coronary intervention.

摘要

Contrast-induced acute kidney injury (CI-AKI) remains an important and potentially avoidable complication after coronary angiography and intervention.1 There is a direct inverse relationship between the estimated glomerular filtration rate (eGFR) and the risk of CI-AKI. In the setting of severely reduced renal filtration, there is greater risk for more sustained intra-renal vasoconstriction, tubular and peritubular stasis of contrast, cellular toxicity, and permanent loss of some functioning nephrons (Fig. I). There is recent appreciation that iodinated contrast stays within the kidney and probably in the peritubular space for a week or more after contrast administration, causing clinical trialists to consider extending postprocedure antioxidants from the traditional 2 up to 8 days. During this prolonged contrast exposure, it is believed that the direct cellular toxicity of iodinated contrast sets up a wavefront of oxidative injury as adjacent renal tubular cells undergo injury and death. Each cell liberates tiny amounts of labile iron from organelles into the interstitial and urinary spaces. Labile iron allows the transfer of oxygen and hydrogen by critical reactions that lead to the generation of peroxides and other reactive oxygen species that then go on to injure adjacent cells.