The Correlation Between Interleukin-10 1082G/A Gene Polimorphism Late Onset with Nephrotoxicity Secondary to Antituberculosis Treatment in Multidrug Resistant Tuberculosis Patients

Harsini Harsini, Reviono Reviono, Umarudin Umarudin

Abstract


Introduction: Tuberculosis controlling programme has become more complex with MDR-TB problem. IL-10 1082G/A gene polimorphism correlates with IL-10 secretion as anti inflammatory cytokine which plays important role in pathogenesis MDR-TB infection. The management of MDR-TB that using aminoglicoside causing nephrotoxic effect to the patients. The protective role of IL-10 from IL-10 1082 G/A genotype to nephrotoxic effect due to canamycin still becomes a prolem nowadays.
Methods: This was a retrspective cohort study of MDR-TB patients who underwent treatment in Dr. Moewardi Hospital in 2011-2015.
Results: There were 89 MDR-TB patients with IL-10 1082 G/A genotype polimorphism included in this study. The proportions of IL-10 1082 G/A genotype were AA genotype 13.48%, GG 4.49%, and GA 82.2%. Interleukin 10 1082 G/A gene polymorphism had no significant correlation with nephrotoxicity onset in MDR-TB patients in Dr. Moewardi hospital.
Conclusions: The onset of nephrotoxicity in IL-10 1082G/A gene polymporphism GG genotype was faster than GA and AA genotype. (J Respir Indo. 2019; 39(4):)

Keywords


MDR-TB, IL-10 1082 G/A genotype polimorphism, nephrotoxicity

References


Katherine F, Annabel B, Anna D, Hannah MD, Dennis F, Inés G, et al. Editors. Global tuberculosis report. France: WHO Library Cataloguing-in-Publication Data. 2013.

Amalia L, Maidatuz Z, Soeroto AY. Comparative Study Of Kanamycin and Capremicin on Potassium Level of Multidrug Resistance Tuberculosis Patientsat a Hospital in Bandung Indonesia. J Int Pharm Pharm Sci. 2016;8:307-10.

World Health Organiation. WHO treatment guidelines for drug-resistant tuberculosis. Switzerland. WHO. 2016:59-72.

Jose AC, Giovani S, Alimuddin Z, Giovani BM. Best drug treatment for multi-drug-resistant and extensively drug-resistant tuberculosis. Lancet Infect Dis. 2010;10:621-9.

Lopez-Novoa JM, Quiros Y, Vicente L, Morales AI, Lopez-Hernandez FJ. New insights into the mechanism of aminoglycoside nephrotoxicity: an integrative point of view. Kidney Int. 2011;79:33–45.

Bell S, Davey P, Nathwani D, Marwick C, Vadiveloo T, Sneddon J, et al. Risk of AKI with gentamicin as surgical prophylaxis. J Am Soc Nephrol. 2014;25:2625–32.

Paquette F, Bernier-Jean A, Brunette V, Ammann H, Lavergne V, Pichette V, et al. Acute Kidney Injury and Renal Recovery with the Use of Aminoglycosides: A Large Retrospective Study. Nephron. 2015;131:153–60.

Waikar SS, Liu KD, Chertow GM. Diagnosis, epidemiology and outcomes of acute kidney injury. J Clin Am Soc Nephrol. 2008;3:844–61.

Chawla LS, Amdur RL, Amodeo S, Kimmel PL, Palant CE. The severity of acute kidney injury predicts progression to chronic kidney disease. Kidney Int. 2011;79: 1361–69.

Morata L, Cobos-Trigueros N, Martinez JA, Soriano A, Almela M, Marco F, et al. Influence of multidrug resistance and appropriate empirical therapy on the 30-day mortality rate of Pseudomonas aeruginosa bacteremia. Antimicrob Agents Chemother. 2012;56:4833–37.

Wargo KA, Edwards JD. Aminoglycoside-induced nephrotoxicity. J Pharm Pract. 2014;27:573–7.

Sinuani I, Averbukh Z, Gitelman I, Rapoport MJ, Sandbank J, Albeck M, et al. Mesangial cells initiate compensatory renal tubular hypertrophy via IL-10 induced TGF beta secretion: effect of the immunomodulator AS101 on this process. Am J Physiol Renal Physiol. 2006;384-94.

Jaber BL, Prereira BJG, Bonventre JV, Balakrishnan VTS. Polymorphism of host response genes: Implications in the pathogenesis and treatment of acute renal failure. Kidney International. 2005;67:14–33.

Anthony TG, Stanislaw PS, Charles HC, Claire M. Risk factors for aminoglycoside associated nephrotoxicity in surgical intensive care unit patients. International Journal of Critical Illness and Injury Science. 2011;1:17-21.

Mulu W, Mekonnen D, Yimer M, Admassu A, Abera B. Risk factors for multidrug resistant tuberculosis patients in Amhara National Regional State. African Health Sciences. 2015;2:368-77.

Singla R, Sharma SK, Mohan A, Makharia G, Sreenivas V, Jha B. Evaluation of risk factors for antituberculosis treatment induced hepatotoxicity. Indian J Med Res. 2010;132:81–86.

Greenberg AS, Obin MS. Obesity and the role of adipose tissue in inflammation and Griffiths, G., Nyström, B., Sable, S. B. and Khuller, G. K. metabolism 1– 4. Am J Clin Nutr. 2006;83:461–465.

Fen W, Yabin Q, Yunxia T, Duizhi C, Pin C, Zhaolin X. Lack of association between cytokine gene polymorphisms and silicosis and pulmonary tuber¬culosis in Chinese iron miners. J of Ocupational Health. 2008;50:445-54.

Asgharzadeh, M; Ghorghanlu, S; Rashedi, J. Association of promoter polymorphism of interleukin-10 and interferon-gamma with tuberculosis in Azeri population of Iran. Iran J Allergy Asthma Immunol. 2016:15(3):167–73.




DOI: https://doi.org/10.36497/jri.v39i4.71

Refbacks

  • There are currently no refbacks.





Jurnal Respirologi Indonesia
pISSN: 0853-7704 - eISSN: 2620-3162
Address: Jalan Cipinang Bunder No. 19, Cipinang, Pulogadung, Jakarta Timur, DKI Jakarta 13240, Indonesia
Phone: +62-21-2247-4845
Email: editor@jurnalrespirologi.org


An official publication by
the Indonesian Society of Respirology (ISR)

Creative Commons License
Creative Commons Attribution-NonCommercial 4.0 International License

Statcounter