Contrast-associated nephropathy (CAN), defined as an increase in serum creatinine levels within 24 to 48 hours of contrast exposure, is a common cause of reversible AKI in the hospital setting. Contrast-induced nephropathy (CIN) includes that subset of CAN in which the kidney injury can be more definitively linked to the contrast. Multiple risk factors have been associated with CAN, but a baseline reduction in eGFR appears most important, especially in patients with AKI and in patients with CKD and an eGFR <30 mL/min/1.73 m2.
CIN is thought to be due to ATN from contrast-induced vasoconstriction, decreased renal blood flow, medullary hypoxia, oxidative stress, and direct tubular cytotoxicity. AKI tends to be nonoliguric, with an FENa <1%. The urinary sediment may be bland or show classic ATN findings.
Preventive strategies for patients at high risk for CIN include minimizing the amount of contrast, using low or iso-osmolar contrast, discontinuing nephrotoxins, and prophylactically administering intravenous isotonic saline. Prophylactic saline should be administered to all patients with an eGFR <30 mL/min/1.73 m2 and should be considered for patients with an eGFR of 30 to 44 mL/min/1.73 m2 who have other risk factors for AKI. A randomized controlled trial demonstrated that oral acetylcysteine was no more effective than placebo for the prevention of CIN. Statins have been shown in observational studies and several randomized controlled trials to prevent CIN by acting as stabilizers of the endothelium and free radical scavengers in a model of ischemic nephropathy. Further studies are needed to establish their benefit. There is no role for prophylactic hemodialysis or hemofiltration following contrast exposure. Treatment of CIN is supportive.