2012;2(1):1-138. 14. Vidt DG, Harris S, McTaggart F, et al. Effect of short-term rosuvastatin treatment on estimated glomerular filtration rate. Am J Cardiol. 2006 Jun 1;97(11):1602-6. PMID: 16728222. 15. Jang JS, Jin HY, Seo JS, et al. Sodium bicarbonate therapy for the prevention of contrast-induced acute kidney injury - a systematic review and meta-analysis. Circ J. 2012;76(9):2255-65. PMID: 22975638. 1 Introduction Background The administration of iodinated contrast media is an essential component of a number of diagnostic and therapeutic procedures that involve radiologic imaging. One important potential side-effect of iodinated contrast administration is contrast-induced nephropathy (CIN, see Appendix A for a list of acronyms), defined as an increase in serum creatinine of more than 25 percent or 0.5 mg/dL within 3 days of intravascular administration of contrast media in the absence of an alternative etiology. 1 This definition of CIN, or variations of it, is the one most commonly used in the past by studies examining the risk, prevention, and treatment of CIN. More recent consensus definitions of acute kidney injury, such as RIFLE2 and AKIN,3 have not yet been used extensively in the CIN literature. Although some guidelines have employed the term "contrast-induced acute kidney injury" (CI-AKI) instead of CIN, the vast majority of the literature has used the older term, CIN, so we will use the older term in our report. The precise mechanism of CIN is not entirely understood. The leading theories are that CIN results from hypoxic injury of the renal tubules induced by renal vasoconstriction or by direct cytotoxic effects of the contrast media.4,5 Some experts have questioned whether acute kidney injury occurring after intravascular administration of contrast media is caused by co-existing risk factors and only coincidentally related to the contrast media, especially if contrast media are administered by the intravenous (IV) route. In a meta-analysis, McDonald et al., 2013 concluded that the incidence of acute kidney injury was similar between patients receiving IV contrast media and patients receiving an imaging procedure without contrast media. Regardless of the precise etiology, however, the development of acute kidney injury after use of intravascular contrast media remains a major concern for clinicians.6 Clinicians often worry about the possibility that intra-vascular administration of contrast media in diagnostic or therapeutic procedures could lead to acute or chronic kidney failure. Indeed, CIN is cited as a leading cause of hospital-acquired kidney failure.7 Although renal function returns to normal in most patients, acute kidney injury may require short-term renal replacement therapy or may lead to chronic kidney disease and a need for long-term renal replacement therapy. Clinicians are concerned about the risk of CIN because of increasing use of contrast media in radiologic and cardiologic procedures, and the high prevalence of populations vulnerable to CIN (i.e., people having chronic kidney disease, diabetes mellitus, or hypertension, as well as the elderly). Various types of imaging studies or procedures use IV or intra-arterial contrast media, including: IV pyelograms; brain, head and neck, body, or coronary computed tomograms (CT); cerebral, cardiac, or peripheral vascular angiograms; and radiologic therapeutic procedures. Contrast media is injected intravenously for CT and intra-arterially for angiograms and related interventional procedures. More than 62 million CT studies were performed in the United States in 2006 and the use of CT tripled between 1996 and 2010, from 52 studies per 1000 patients to 149 studies per 1000 patients.8 The reported incidence of CIN varies, but a reasonable overall estimate is that it occurs in about 2 percent of patients receiving intra-vascular contrast media.7 Variation in the populations studied makes it difficult to determine whether the incidence of CIN has increased over time. Most of the estimates are derived from invasive angiographic studies, over the last few decades, using intra-arterial contrast media, which may have a higher risk of CIN than imaging studies using IV contrast media. One problem in determining the precise incidence of CIN is that many patients do not remain hospitalized for enough time after contrast administration to make the 2 diagnosis. In addition, the use of serum creatinine as a marker of renal function has its limitations. It is often difficult to exclude other possible etiologies of elevations in serum creatinine. Furthermore, the incidence may vary according to the osmolality of contrast media used. Although there is consensus that the risk of CIN is highest with high-osmolar contrast media (HOCM), which has an osmolality five to eight times higher than plasma osmolality, HOCM is no longer used in clinical practice. It is unclear whether or not the risk of CIN differs between low-osmolar contrast media (LOCM), which has an osmolality two to three times plasma osmolality, and iso-osmolar contrast media (IOCM), which is isotonic to plasma. It is also often difficult to distinguish the effects of contrast media from the effects of physiologic confounders that could elevate the serum creatinine in patients undergoing radiologic studies. For example, blood flow to the kidneys could be compromised by emboli or vascular compression from catheter manipulation.9,10