Minimizing the Renal Toxicity of Iodinated Contrast

Abstract

A substantial proportion of adults with coronary disease are at risk for contrast-induced acute kidney injury (CI-AKI), manifested primarily by underlying chronic kidney disease, defined as an estimated glomerular filtration rate <60 mL · min−1 · /1.73−2.1 Although patients commonly understand that they have heart disease, studies have shown that <10% of those with chronic kidney disease are actually aware of this problem; thus, if not emphasized by the cardiologist during the consent before angiography, CI-AKI may come as a surprise to patients and their families after the procedure.2–4 All forms of intravascular iodinated contrast are very water soluble, freely filtered by the glomerulus, and avidly taken up by renal tubular cells in the loop of Henle, and are retained in patients with chronic kidney disease within tubular cells and the peritubular space for ≈7 days where there is direct oxidative cellular damage, sloughing of renal tubular cells and brush border material, and acute tubular dysfunction.5 Thus, the interest in reducing CI-AKI and its translation, if …