Contrast-Induced Acute Kidney Injury
Peter A. McCullough, MD, MPH, FACC, FACP, FAHA, FCCP*
Divisions of Cardiology, Nutrition, and Preventive Medicine, William Beaumont Hospital, Royal Oak, Michigan.

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Figure 1 Postulated Pathophysiology of Contrast-Induced AKI
In the presence of a reduced nephron mass, the remaining nephrons are vulnerable to injury. Iodinated contrast, after causing a brief (minutes) period of vasodilation, causes sustained (hours to days) intrarenal vasoconstriction and ischemic injury. The ischemic injury sets off a cascade of events largely driven by oxidative injury causing death of renal tubular cells. If a sufficient mass of nephron units are affected, then a recognizable rise in serum creatinine will occur.
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Figure 2 Risk of Contrast-Induced AKI According to Baseline Renal Function (eGFR or CrCl ml/min)
Contrast-induced acute kidney injury (AKI) was defined as serum creatinine increase of 25% and/or 0.5 mg/dl and is shown separately for patients with (solid circles) and without (open circles) diabetes. CrCl = creatinine clearance; eGFR = estimated glomerular filtration rate. Data adapted from McCullough et al. (12).
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Figure 3 Rates of Contrast-Induced AKI in a Meta-Analysis of 16 Trials of Iso-Osmolar Iodixanol
Relative risk reductions (RRRs) are for iso-osmolar (IOCM) compared with low-osmolar contrast media (LOCM). CKD = baseline chronic kidney disease defined as an estimated creatinine clearance <60 ml/min; DM = diabetes mellitus. Data adapted from McCullough et al. (47).
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Figure 4 Advanced Algorithm for Management of Patients Receiving Iodinated Contrast Media
ACS = acute coronary syndromes; bid = twice daily; Cr = creatinine; DM = diabetes mellitus; IV = intravenous; NAC = N-acetylcysteine; NSAIDs = nonsteroidal anti-inflammatory drugs; PGE1 = prostaglandin E1; po = by mouth; other abbreviations as in Figure 2.
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