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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
Author(s) -
Guerchicoff Alejandra,
Stone Gregg W.,
Mehran Roxana,
Xu Ke,
Nichols Dru,
Claessen Bimmer E.,
Guagliumi Giulio,
Witzenbichler Bernhard,
Henriques José P.S.,
Dangas George D.
Publication year - 2015
Publication title -
catheterization and cardiovascular interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.988
H-Index - 116
eISSN - 1522-726X
pISSN - 1522-1946
DOI - 10.1002/ccd.25620
Subject(s) - medicine , percutaneous coronary intervention , myocardial infarction , cardiology , acute kidney injury , conventional pci , biomarker , acute coronary syndrome , cystatin c , renal function , biochemistry , chemistry
Objectives Contrast‐induced acute kidney injury (CI‐AKI) may occur after percutaneous coronary intervention (PCI). Methods We evaluated patients with ST‐elevation myocardial infarction (STEMI) undergoing emergency PCI with serial biomarkers. Results Of 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. Conclusions The 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.