TY - JOUR
T1 - Analysis of Biomarkers for Risk of Acute Kidney Injury After Primary Angioplasty for Acute ST-Segment Elevation Myocardial Infarction: Results of the HORIZONS-AMI Trial
AU - Guerchicoff, Alejandra
AU - Stone, Gregg W.
AU - Mehran, Roxana
AU - Xu, Ke
AU - Nichols, Dru
AU - Claessen, Bimmer E.
AU - Guagliumi, Giulio
AU - Witzenbichler, Bernhard
AU - Henriques, José P. S.
AU - Dangas, George D.
PY - 2015
Y1 - 2015
N2 - 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
AB - 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
U2 - https://doi.org/10.1002/ccd.25620
DO - https://doi.org/10.1002/ccd.25620
M3 - Article
C2 - 25130788
SN - 1522-1946
VL - 85
SP - 335
EP - 342
JO - Catheterization and cardiovascular interventions
JF - Catheterization and cardiovascular interventions
IS - 3
ER -