Contrast-Induced Acute Kidney Injury

Case Presentation : A 63-year-old man with prior mitral valve repair, hyperlipidemia, hypertension, and mild chronic renal insufficiency (creatinine 1 year earlier, 1.2 mg/dL) presents to the emergency department with progressive dyspnea on exertion and new anterior T-wave inversions. Subsequent laboratory testing confirms a myocardial infarction (troponin I, 11.0 ng/mL) and worsening renal insufficiency in the setting of recently being started on chlorthalidone for hypertension (creatinine, 2.7 mg/dL). Diuretics are discontinued; intravenous fluids are infused; and therapy for an acute coronary syndrome, including aspirin, clopidogrel, nitrates, and intravenous unfractionated heparin, is initiated. After 48 hours, creatinine improves to 1.8 mg/dL (estimated glomerular filtration rate, 46 mL/min), and the patient undergoes cardiac catheterization with iopamidol (Isovue, Bracco Diagnostics Inc, Princeton, NJ) contrast after receiving 1 hour of prophylactic sodium bicarbonate infusion. A complex bifurcation lesion of the left anterior descending artery/first diagonal branch is identified (Figure 1A). What is this patient's risk of contrast-induced acute kidney injury (CI-AKI), and which measures may modify that risk significantly? This Clinician Update reviews the recent literature on the acute kidney injury that follows the administration of iodinated contrast medium.Figure 1. A, A complex culprit lesion in the left anterior descending artery (LAD) and first diagonal branch (D1). B, After 250 cm3 iopamidol contrast dye, successful drug-eluting stent placement in the LAD-D1 bifurcation lesion.Patients at risk for CI-AKI have comorbidities that will exacerbate the primary pathogenesis of the injury: contrast-induced vasoconstriction leading to diminished blood flow to the renal medulla. These comorbidities include diabetes mellitus, congestive heart failure, acute hypotension (requiring pressors or intra-aortic balloon pump), ST-elevation myocardial infarction, and volume depletion. Patients with chronic kidney disease are also at risk for contrast-induced acute kidney injury because compensatory mechanisms to maintain filtration function are diminished, and a smaller number of nephrons must excrete …