Foxp3 Serum Levels in Contrast Induced Nephrophaty Patients After the Administration of Contrast Media
International Journal of Biomedical Materials Research
Volume 5, Issue 2, April 2017, Pages: 25-28
Received: Apr. 4, 2017; Accepted: Apr. 21, 2017; Published: Jun. 1, 2017
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Authors
Yuyun Widaningsih, Department of Clinical Pathology, Hasanuddin University, Makassar City, Indonesia
Rosdiana Natsir, Department of Biochemistry, Hasanuddin University, Makassar City, Indonesia
Mansyur Arif, Department of Clinical Pathology, Hasanuddin University, Makassar City, Indonesia
Uleng Bahrun, Department of Clinical Pathology, Hasanuddin University, Makassar City, Indonesia
Hasyim Kasim, Department of Internal Medicine, Hasanuddin University, Makassar City, Indonesia
Nursin Abdul Kadir, Department of Clinical Pathology, Hasanuddin University, Makassar City, Indonesia
Fitri Hamka, Department of Clinical Pathology, Hasanuddin University, Makassar City, Indonesia
Nadyah Haruna, Department of Medicine, UIN Alauddin University, Makassar City, Indonesia
Mochammad Hatta, Department of Immunology and Biomolecular, Hasanuddin University, Makassar City, Indonesia
Andi Nilawati Usman, Halal Center of Public Health, Hasanuddin University, Makassar City, Indonesia
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Abstract
Percutaneous Coronary Intervention (PCI) procedure increases the risk of inflammation risk and represents adverse effects to immune system in the human body. One of the functions in the human body in maintaining the balance of immune system is Foxp3 of regulatory T cells and the function of Foxp3 is seldom to be the subject of study in coronary patients from the administration of contrast agents after PCI. This study was conducted to analyze the comparison Foxp3 levels of regulatory T cells in blood serums in patients who experienced contrast induced nephrophaty (CIN) after PCI procedure for both the CIN group and the non-CIN group. The population of coronary patients after PCI. The sample size was 20 patients that consisted of 10 patients who experienced CIN and 10 patients who experienced the CIN group. Categorization of both the CIN and non-CIN group used Kidney Disease Improving Global Outcomes (KDIGO) and detection of Foxp3 levels in blood serums using Enzyme-linked immunosorbent assay (ELISA) technique. Result of this study indicated that the characteristics of patients between the CIN group and the non-CIN group did not reveal significant difference, except for the characteristic of age. Results of the analysis by using statistical pair and non-pair t-test showed that patients for both the CIN group and non-CIN group experienced significant reduction of Foxp3 levels of regulatory T cells in their blood serums. This indicated that the PCI procedure indeed led to inflammation and Foxp3 levels and it could not be used as the specific marker for CIN incidence, but it should be mediated by the inflammation marker.
Keywords
Percutaneous Coronary Intervention, Contrast Induced Nephrophaty, Foxp3
To cite this article
Yuyun Widaningsih, Rosdiana Natsir, Mansyur Arif, Uleng Bahrun, Hasyim Kasim, Nursin Abdul Kadir, Fitri Hamka, Nadyah Haruna, Mochammad Hatta, Andi Nilawati Usman, Foxp3 Serum Levels in Contrast Induced Nephrophaty Patients After the Administration of Contrast Media, International Journal of Biomedical Materials Research. Vol. 5, No. 2, 2017, pp. 25-28. doi: 10.11648/j.ijbmr.20170502.12
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Copyright © 2017 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
References
[1]
Garcia, S., B. Ko, and S. Adabag, Contrast-induced nephropathy and risk of acute kidney injury and mortality after cardiac operations. Ann Thorac Surg, 2012. 94 (3): p. 772-6.
[2]
Shoukat, S., et al., Contrast-induced nephropathy in patients undergoing percutaneous coronary intervention. Cardiol Res Pract, 2010. 2010.
[3]
Sadat, U., Radiographic contrast-media-induced acute kidney injury: pathophysiology and prophylactic strategies. ISRN Radiol, 2013. 2013: p. 496438.
[4]
Schrier, R. W., et al., Acute renal failure: definitions, diagnosis, pathogenesis, and therapy. J Clin Invest, 2004. 114 (1): p. 5-14.
[5]
Bonventre, J. V. and L. Yang, Cellular pathophysiology of ischemic acute kidney injury. J Clin Invest, 2011. 121 (11): p. 4210-21.
[6]
Kinsey, G. R., R. Sharma, and M. D. Okusa, Regulatory T cells in AKI. J Am Soc Nephrol, 2013. 24 (11): p. 1720-6.
[7]
Kinsey, G. R. and M. D. Okusa, Expanding role of T cells in acute kidney injury. Curr Opin Nephrol Hypertens, 2014. 23 (1): p. 9-16.
[8]
Rudensky, A. Y., Regulatory T cells and Foxp3. Immunol Rev, 2011. 241 (1): p. 260-8.
[9]
Chong, E., et al., Risk factors and clinical outcomes for contrast-induced nephropathy after percutaneous coronary intervention in patients with normal serum creatinine. Ann Acad Med Singapore, 2010. 39 (5): p. 374-80.
[10]
Ando, G., et al., Age, glomerular filtration rate, ejection fraction, and the AGEF score predict contrast-induced nephropathy in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention. Catheter Cardiovasc Interv, 2013. 82 (6): p. 878-85.
[11]
Munk, P. S., et al., Inflammatory response to percutaneous coronary intervention in stable coronary artery disease. J Thromb Thrombolysis, 2011. 31 (1): p. 92-8.
[12]
Valencia, X., et al., TNF downmodulates the function of human CD4+CD25hi T-regulatory cells. Blood, 2006. 108 (1): p. 253-61.
[13]
Nie, H., et al., Phosphorylation of FOXP3 controls regulatory T cell function and is inhibited by TNF-alpha in rheumatoid arthritis. Nat Med, 2013. 19 (3): p. 322-8.
[14]
Emoto, T., et al., Regulatory/Effector T-Cell Ratio Is Reduced in Coronary Artery Disease. Circulation Journal, 2014. 78 (12): p. 2935-2941.
[15]
Salgado Filho, W., et al., [Intracoronary inflammatory markers after percutaneous coronary interventions]. Arq Bras Cardiol, 2005. 85 (3): p. 180-5.
[16]
Saadeddin, S. M. and M. A. Habbab, Percutaneous coronary intervention in the context of systemic inflammation: more injury and worse outcome. Med Sci Monit, 2003. 9 (8): p. Ra193-7.
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