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Radiocontrast was first described to cause nephrotoxicity in the 1960s.1,2 Contrast-induced nephropathy (CIN), now termed contrast-induced acute kidney injury (CI-AKI), is likely to increase in frequency over the next 10 to 15 years. This rise is largely due to increasing use of radiocontrast studies in patients who are older, sicker, or have attendant comorbidities such as diabetes mellitus, renal failure, cardiac failure, and volume depletion.3 CI-AKI is currently described as the third most common cause of hospital acquired renal failure, accounting for approximately 11% of cases.4 The incidence of CI-AKI reported in the literature has ranged between 1% and 45%, largely depending on the comorbidities of the study population, the clinical scenario in which the contrast is given, and the parameters used to define CI-AKI.5 With more than a million radiocontrast procedures performed annually in the United States, the incidence of CI-AKI is approximately 150,000 cases per year. At least 1% of these episodes require dialysis therapy (in half of patients, it will be permanent) with prolongation of hospital stay to an average of 17 days, with an additional cost of approximately $32 million annually. For episodes that do not require dialysis, the average prolongation of the hospital stay is 2 days (at $500 per day), and this translates to an added cost of $148 million annually.6,7 The incidence and costs are higher in critically ill patients, who have associated comorbidities such as hypotension, hypovolemia, diabetes, and congestive heart failure.

This chapter will first examine the important renal complications of contrast media. This will be followed by an evaluation of laboratory investigations that provide insights into the pathogenesis of this disorder. The last section deals with 2 important clinical issues: (1) the use of low-osmolality radiocontrast agents specifically to reduce the incidence of CI-AKI and (2) adjunctive methods currently used to prevent the development of CI-AKI.


The obesity pandemic is a central driver of the dysmetabolic syndrome, hypertension, and diabetes. It is thus anticipated that there will soon occur a secondary epidemic of combined chronic kidney disease (CKD) and cardiovascular disease (CVD).8 Among patients with diabetes for 25 years or more, the prevalence of diabetic nephropathy in type 1 and type 2 diabetes is 57% and 48%, respectively. Approximately half of all cases of end-stage renal disease (ESRD) are due to diabetic nephropathy, with most of these cases driven by obesity-related type 2 diabetes and hypertension.9 With the graying of America and cardiovascular care shifting toward the elderly, the imperative thus exists to understand the relationship between decreasing levels of renal function as a major adverse prognostic factor in cardiac patients. AKI after contrast exposure as the most proximal renal event is predictable and highlights an opportunity for preventive measures outlined later in this chapter.


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