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      The Predictive Value of Myeloperoxidase for Contrast-Induced Nephropathy After Percutaneous Coronary Intervention in Patients with Acute Myocardial Infarction

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          Abstract

          Background

          Higher serum myeloperoxidase (MPO) in patients with acute coronary syndrome is associated with adverse cardiovascular outcomes. Contrast-induced nephropathy (CIN) is associated with worse prognosis in patients with coronary artery disease following angiography. We have no idea whether patients with higher serum myeloperoxidase have a higher risk of CIN in acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI).

          Methods

          This study involved 436 consecutive patients with AMI who had received PCI. Serum MPO levels were determined using enzyme-linked immunosorbent assay before administration of contrast media. Multivariate logistic regression analysis was used to analyze the independent risk factors for CIN after univariate analysis. The receiver operator characteristic (ROC) analysis was performed to evaluate the predictive value of MPO for CIN.

          Results

          Among the 436 patients, 79 individuals (18.1%) suffered CIN after the PCI procedure. Patients who developed CIN had significantly higher MPO levels compared to those who did not ([203.8 (150.6–276.2)] versus [138.5 (129.9–149.2)]; p<0.001). Multivariate logistic regression analysis revealed that MPO level (OR 1.023, 95% CI: 1.017–1.029, p<0.001) was an independent risk factor for the incidence of CIN after adjusting for the baseline information, blood indicators and angiography procedural parameters. The area under the ROC curve for predicting CIN of MPO was 0.848, and the optimum cutoff point of MPO was 147.38ug/L; the sensitivity and specificity were 82.3% and 72.3%, respectively.

          Conclusion

          The results show that MPO is independently associated with an increased risk of CIN with AMI patients undergoing PCI. Further studies are needed to verify these results.

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          Most cited references35

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          Contrast induced nephropathy: updated ESUR Contrast Media Safety Committee guidelines.

          The Contrast Media Safety Committee (CMSC) of the European Society of Urogenital Radiology (ESUR) has updated its 1999 guidelines on contrast medium-induced nephropathy (CIN). Topics reviewed include the definition of CIN, the choice of contrast medium, the prophylactic measures used to reduce the incidence of CIN, and the management of patients receiving metformin. Key Points • Definition, risk factors and prevention of contrast medium induced nephropathy are reviewed. • CIN risk is lower with intravenous than intra-arterial iodinated contrast medium. • eGFR of 45 ml/min/1.73 m (2) is CIN risk threshold for intravenous contrast medium. • Hydration with either saline or sodium bicarbonate reduces CIN incidence. • Patients with eGFR ≥ 60 ml/min/1.73 m (2) receiving contrast medium can continue metformin normally.
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            Mediators of Inflammation in Acute Kidney Injury

            Acute kidney injury (AKI) remains to be an independent risk factor for mortality and morbidity. Inflammation is now believed to play a major role in the pathopathophysiology of AKI. It is hypothesized that in ischemia, sepsis and nephrotoxic models that the initial insult results in morphological and/or functional changes in vascular endothelial cells and/or in tubular epithelium. Then, leukocytes including neutrophils, macrophages, natural killer cells, and lymphocytes infiltrate into the injured kidneys. The injury induces the generation of inflammatory mediators like cytokines and chemokines by tubular and endothelial cells which contribute to the recruiting of leukocytes into the kidneys. Thus, inflammation has an important role in the initiation and extension phases of AKI. This review will focus on the mediators of inflammation contributing to the pathogenesis of AKI.
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              Myeloperoxidase and cardiovascular disease.

              Myeloperoxidase (MPO) is a leukocyte-derived enzyme that catalyzes the formation of a number of reactive oxidant species. In addition to being an integral component of the innate immune response, evidence has emerged that MPO-derived oxidants contribute to tissue damage during inflammation. MPO-catalyzed reactions have been attributed to potentially proatherogenic biological activities throughout the evolution of cardiovascular disease, including during initiation, propagation, and acute complication phases of the atherosclerotic process. As a result, MPO and its downstream inflammatory pathways represent attractive targets for both prognostication and therapeutic intervention in the prophylaxis of atherosclerotic cardiovascular disease.
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                Author and article information

                Journal
                Int J Gen Med
                Int J Gen Med
                ijgm
                ijgm
                International Journal of General Medicine
                Dove
                1178-7074
                30 April 2021
                2021
                : 14
                : 1621-1629
                Affiliations
                [1 ]Department of Cardiology, Zhongda Hospital of Southeast University Medical School , Nanjing, 210009, People’s Republic of China
                Author notes
                Correspondence: Gaoliang Yan; Genshan Ma Department of Cardiology, Zhongda Hospital of Southeast University Medical School , No. 87 Dingjiaqiao, Gulou District, Nanjing, 210009, People’s Republic of ChinaTel/Fax +86 25 83262413; +86 25 83262410 Email yan_seu@hotmail.com; magenshan@hotmail.com
                Article
                303678
                10.2147/IJGM.S303678
                8096440
                33958892
                accebbcd-a368-499f-9b4e-5881fd9469f4
                © 2021 Yan et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 28 January 2021
                : 12 April 2021
                Page count
                Figures: 3, Tables: 11, References: 35, Pages: 9
                Categories
                Original Research

                Medicine
                myocardial infarction,contrast-induced nephropathy,myeloperoxidase,percutaneous coronary intervention

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