Key result
Patients who developed acute kidney injury after primary PCI for STEMI had significantly higher levels of B-type natriuretic peptide at hospital discharge compared to those without AKI (1975.5 vs 976.1 pg/mL, p=0.0002), along with elevated D-dimer, CRP, and other inflammatory biomarkers.
Why the study?
Contrast-induced acute kidney injury (CI-AKI) may occur after PCI for STEMI, but the association with serial biomarker changes was unclear.
Are specific serial biomarkers associated with the development of contrast-induced acute kidney injury in STEMI patients undergoing emergency PCI?
Observational (n=390)
Open-label
Yes
Are specific serial biomarkers associated with the development of contrast-induced acute kidney injury in STEMI patients undergoing emergency PCI?
Absolute Event Rate: 1975.5% vs 976.1%
p-value: p=0.0002
Elevated levels of BNP, inflammatory, and procoagulant biomarkers are associated with the development of contrast-induced acute kidney injury after primary PCI for STEMI.
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.
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Guerchicoff et al. (2014) conducted an observational in ST-segment elevation myocardial infarction (STEMI) (n=390). Acute kidney injury (AKI) vs. No AKI was evaluated on B-type natriuretic peptide (BNP) levels at hospital discharge (pg/mL) (p=0.0002). Patients who developed acute kidney injury after primary PCI for STEMI had significantly higher levels of B-type natriuretic peptide at hospital discharge compared to those without AKI (1975.5 vs 976.1 pg/mL, p=0.0002), along with elevated D-dimer, CRP, and other inflammatory biomarkers.
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