• Alejandra Guerchicoff, Gregg W Stone, Roxana Mehran, Ke Xu, Dru Nichols, Bimmer E Claessen, Giulio Guagliumi, Bernhard Witzenbichler, José P S Henriques, and George D Dangas.
• Cardiovascular Research Foundation, New York, New York.
• Catheter Cardiovasc Interv. 2015 Feb 15; 85 (3): 335-42.

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.© 2014 Wiley Periodicals, Inc.

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