Chapter 23. Interventions To Prevent Contrast-Induced Acute Kidney Injury

How Important Is the Problem? Over 70 million computed tomography (CT) scans are performed yearly in the United States, approximately half of which use iodinated radiocontrast media, and over 2 million patients undergo other studies using radiocontrast media such as coronary angiograms. Contrastinduced acute kidney injury (CI-AKI) is one of the major risks of procedures using radiocontrast media. CI-AKI is generally defined by laboratory criteria: biochemical CI-AKI is usually defined as an increase in serum creatinine of 25%, or an absolute increase of 0.5 mg/dl, within 2-5 days after receiving contrast. A prospective study found that the incidence of CI-AKI by this definition was 7.7% in patients with impaired baseline kidney function (defined as an estimated glomerular filtration rate of less than 60 mL/min/ 1.73 m), ranging from 6.5% in patients undergoing CT scans to 13.2% in patients undergoing non-coronary angiography. Risk factors for CI-AKI include chronic kidney disease (CKD) of any cause, especially in diabetic patients. Other risk factors include intravascular volume depletion and disease states associated with decreased effective circulating volume and renal perfusion, such as congestive congestive heart failure (CHF) and liver failure, and concominant use of nephrotoxic medications, particularly non-steroidal anti-inflammatory drugs (NSAIDs). Procedural risk factors also play a role, with larger volumes of contrast media, intra-arterial contrast administration (such as in coronary angiography), and use of high-osmolarity contrast media all independently associated with elevated risk for CI-AKI. Patients with normal baseline kidney function have minimal risk of CI-AKI. Although biochemical CI-AKI is commonly documented, the link between laboratory abnormalities and clinical outcomes is controversial. Several studies have shown an independent link between CI-AKI diagnosis in hospitalized patients and subsequent increases in length of stay, progression to end-stage renal disease, and shortand long-term mortality. However, causality is difficult to determine despite the presence of this association, because many factors that predispose to CI-AKI (especially CHF and CKD) also are associated with adverse clinical outcomes independent of CI-AKI development. In addition, AKI of any cause is associated with worsened shortand long-term outcomes in hospitalized patients. In prospective studies, CIAKI has been found as an asymptomatic laboratory abnormality in the vast majority of patients. Only 1 of 660 patients in a 2008 study by Weisbord et al. required kidney dialysis after receiving contrast.