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 …

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