期刊
CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS
卷 85, 期 3, 页码 335-342出版社
WILEY-BLACKWELL
DOI: 10.1002/ccd.25620
关键词
acute kidney injury; angioplasty; STEMI; biomarkers
资金
- Cardiovascular Research Foundation
- Boston Scientific
- Medicines Company
- Bristol-Myers Squibb/Sanofi
- Eli Lilly and Company/Daiichi-Sankyo
- Abbott Vascular
ObjectivesContrast-induced acute kidney injury (CI-AKI) may occur after percutaneous coronary intervention (PCI). MethodsWe evaluated patients with ST-elevation myocardial infarction (STEMI) undergoing emergency PCI with serial biomarkers. ResultsOf the 390 patients enrolled in the HORIZONS-AMI biomarker substudy, 56 (14.3%) developed AKI. In the AKI group, the levels of B-type natriuretic peptide were consistently higher than in the no-AKI group at baseline (P=0.0327), hospital discharge (P=0.0002), 30-day follow-up (P=0.0193), and 1-year follow-up (P=0.031). At hospital discharge, the AKI group had elevated biomarkers compared to the no-AKI group: D-dimer (P=0.0066), C-reactive protein (P=0.0468), endothelial cell-selective adhesion molecule (P=0.0169), adiponectin (P=0.0346), and von Willebrand factor (P=0.0168); there was also a trend toward higher cystatin C (P=0.0585) in the AKI group. Similar correlations between biomarker panel increase and the development of CI-AKI were consistent at baseline, 30-day, and 1-year follow-up. Chemokine (C-C motif) ligand 23 showed an opposite pattern with an increase at all time points in the no-AKI compared to the AKI group. ConclusionsThe risk of CI-AKI after primary PCI for STEMI may be associated with hemostatic imbalances, activation of procoagulants, decreased endogenous anticoagulants, enhanced inflammation, platelet activation, or decreased fibrinolytic activity. (c) 2014 Wiley Periodicals, Inc.
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