Contrast-Induced Nephropathy

Abstract

Contrast medium–induced nephropathy (CIN) is a common cause of acute renal dysfunction. During the past few years, several publications have provided clinical and experimental data on this topic. Our review focuses on 4 major concerns of CIN relevant in clinical practice: (1) What is the evidence that CIN is a clinically relevant and a dangerous condition for the patient? (2) Is there a difference in CIN rate among different contrast media, and how is that related to the physicochemical properties of different available contrast media? (3) What is the evidence that periprocedural hydration is an effective, appropriate, and safe method to prevent CIN? (4) What is the evidence for the use of a drug, in particular acetylcysteine, to prevent CIN? CIN has gained increased attention in the clinical setting, particularly during cardiac intervention but also in many other radiological procedures in which iodinated contrast media are used. There is at present good clinical evidence from well-controlled randomized studies that CIN is a common cause of acute renal dysfunction.1,2 CIN is the acute deterioration of renal function after parenteral administration of radiocontrast media in the absence of other causes. CIN is generally defined as an increase in serum creatinine concentration of >0.5 mg/dL (>44 μmol/L) or 25% above baseline within 48 hours after contrast administration.3–7 Although the exact mechanisms of CIN have yet to be fully elucidated, several causes have been described. Increased adenosine-, endothelin-, and free radical–induced vasoconstriction and reduced nitric oxide– and prostaglandin-induced vasodilatation have been observed. These mechanisms cause ischemia in the deeper portion of the outer medulla, an area with high oxygen requirements and remote from the vasa recta supplying the renal medulla with blood. Contrast agents also have direct toxic effects on renal tubular cells, causing vacuolization, altered mitochondrial function, and apoptosis.8 Atopy …