Jiri Parenica1,2, Petr Kala1,2, Alexandre Mebazaa3,4,5, Simona Littnerova6, Klara Benesova6, Josef Tomandl7, Monika Goldbergová Pavkova8, Jiří Jarkovský6, Jindrich Spinar1,2, Marie Tomandlova7, Milan Dastych9,10, Can Ince11, Katerina Helanova1,2, Martin Tesak1,2, Martin Helan2,12,13, Petr Lokaj14,15, Matthieu Legrand3,4,5,16. 1. Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czechia. 2. Faculty of Medicine, Masaryk University, Brno, Czechia. 3. Université Paris Diderot, PRES Sorbonne Paris Cité, Paris, France. 4. Department of Anaesthesiology and Critical Care and Burn Unit, APHP, Saint Louis Lariboisière University Hospitals, Paris, France. 5. U 942 INSERM, Paris, France. 6. Institute of Biostatistics and Analyses, Faculty of Medicine, Masaryk University, Brno, Czechia. 7. Department of Biochemistry, Faculty of Medicine, Masaryk University, Brno, Czechia. 8. Institute of Pathological Physiology, Faculty of Medicine, Masaryk University, Brno, Czechia. 9. Department of Biochemistry, University Hospital Brno, Brno, Czechia. 10. Department of Laboratory Methods, Faculty of Medicine, Masaryk University, Brno, Czechia. 11. Department of Translational Physiology, Academic Medical Center, Amsterdam, The Netherlands. 12. Department of Anaesthesiology and Intensive Care, St Anne's University Hospital, Brno, Czechia. 13. Intensive Care Research, International Clinical Research Centre (ICRC), Brno, Czechia. 14. Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czechia, alveus@seznam.cz. 15. Faculty of Medicine, Masaryk University, Brno, Czechia, alveus@seznam.cz. 16. F-CRIN-INI-CRCT Network, Nancy, France.
Abstract
BACKGROUND/AIMS: The pathophysiology of acute kidney injury (AKI) in ST-elevation myocardial infarction (STEMI) patients remains poorly explored. The involvement of the nitric oxide (NO) pathway has been demonstrated in experimental ischemic AKI. The aim of this study was to assess the predictive value of circulating biomarkers of the NO pathway for AKI in STEMI patients. METHODS: Four hundred and twenty-seven STEMI patients treated with primary percutaneous coronary intervention were included. The primary end point was AKI. Biomarkers of the NO pathway (plasma superoxide dismutase [SOD], uric acid, nitrite/nitrate [NOx], neopterin) as well as cardiac biomarkers (B-type natriuretic peptide [BNP] and troponin) were sampled 12 h after admission. The predictive value of circulating biomarkers was evaluated in addition to the multivariate clinical model. RESULTS: AKI developed in 8.9% of patients. The 3-month mortality was significantly higher in patients with AKI (34.2 vs. 4.1%; p < 0.001). SOD, uric acid, NOx, neopterin, BNP and troponin were significantly associated with the development of AKI (area under curve [AUC]-receiver operating curve [ROC] ranging between 0.70 and 0.81). In multivariate analysis cardiogenic shock, neopterin, NOx and troponin were independent predictors of AKI. AUC-ROC of the association of multibiomarkers and clinical model was 0.90 and outperformed the predictive value of the clinical model alone. OR of NOx ≥45 µmol/L was 8.0 (95% CI 3.1-20.6) for AKI. CONCLUSION: Biomarkers of the NO pathway are associated with the development of AKI in STEMI patients. These results provide insights into the pathophysiology of AKI and may serve at developing preventing strategies for AKI targeting this pathway.
BACKGROUND/AIMS: The pathophysiology of acute kidney injury (AKI) in ST-elevation myocardial infarction (STEMI) patients remains poorly explored. The involvement of the nitric oxide (NO) pathway has been demonstrated in experimental ischemicAKI. The aim of this study was to assess the predictive value of circulating biomarkers of the NO pathway for AKI in STEMI patients. METHODS: Four hundred and twenty-seven STEMI patients treated with primary percutaneous coronary intervention were included. The primary end point was AKI. Biomarkers of the NO pathway (plasma superoxide dismutase [SOD], uric acid, nitrite/nitrate [NOx], neopterin) as well as cardiac biomarkers (B-type natriuretic peptide [BNP] and troponin) were sampled 12 h after admission. The predictive value of circulating biomarkers was evaluated in addition to the multivariate clinical model. RESULTS:AKI developed in 8.9% of patients. The 3-month mortality was significantly higher in patients with AKI (34.2 vs. 4.1%; p < 0.001). SOD, uric acid, NOx, neopterin, BNP and troponin were significantly associated with the development of AKI (area under curve [AUC]-receiver operating curve [ROC] ranging between 0.70 and 0.81). In multivariate analysis cardiogenic shock, neopterin, NOx and troponin were independent predictors of AKI. AUC-ROC of the association of multibiomarkers and clinical model was 0.90 and outperformed the predictive value of the clinical model alone. OR of NOx ≥45 µmol/L was 8.0 (95% CI 3.1-20.6) for AKI. CONCLUSION: Biomarkers of the NO pathway are associated with the development of AKI in STEMI patients. These results provide insights into the pathophysiology of AKI and may serve at developing preventing strategies for AKI targeting this pathway.
Authors: Martin Helan; Jan Malaska; Josef Tomandl; Jiri Jarkovsky; Katerina Helanova; Klara Benesova; Michal Sitina; Milan Dastych; Tomas Ondrus; Monika Pavkova Goldbergova; Roman Gal; Petr Lokaj; Marie Tomandlova; Jiri Parenica Journal: Antioxidants (Basel) Date: 2022-03-26