Drug-induced Nephropathy and Molecular Patterns of Oxidative Stress

Authors

  • Valentina Lee Department of Internal Diseases, Karaganda Medical University, Karaganda-City, Kazakhstan
  • Ryszhan Bakirova Department of Internal Diseases, Karaganda Medical University, Karaganda-City, Kazakhstan
  • Larissa Muravlyova Department of Biochemistry, Karaganda Medical University, Karaganda-City, Kazakhstan
  • Zhanara Turkhanova Department of Internal Diseases, Karaganda Medical University, Karaganda-City, Kazakhstan
  • Anar Rakhmetova Department of Defectology, Karaganda State University, Karaganda-City, Kazakhstan

DOI:

https://doi.org/10.3889/oamjms.2020.3559

Keywords:

oxidative stress, drug-induced nephropathy, modified proteins, nonsteroidal anti-inflammatory drugs, psychotropic drugs

Abstract

BACKGROUND: Drug-induced kidney disorder is a frequent adverse event which contributes to morbidity and even incapacitation. Our current knowledge of drug-induced kidney disease is limited due to varying definitions of kidney injury, incomplete assessment of concurrent risk factors, and lack of long term outcome reporting.

AIM: The discovery and development of novel biomarkers and local (renal) response mechanisms, which can diagnose kidney damage earlier and more accurately, are needed for effective prevention of drug-induced nephrotoxicity.

METHODS: Forty patients from 22 to 50 years old with drug-induced nephropathy (43 females, 27 males) were included in the study. The determination of oxidative stress modifications as advanced oxidation protein products (AOPPs), protein reactive carbonyl derivatives (PRCD), methylglyoxal, and catalase (CAT) level were assayed. AOPP was rated in blood plasma through the Witko-Sarsat (1996) method, PRCD by Levine (2000) method, methylglyoxal through the Racker (1963) method, CAT was evaluated with Koroljuk (1988) and Aebi (1984) methods. Conditionally, 30 healthy-matched persons were included in the control group.

RESULTS: In psychotropic and nonsteroidal anti-inflammatory drugs (NSAID) drug-induced nephropathy patients, there was a tendency to increase the concentration of AOPP in blood plasma, PRCD, and methylglyoxal in erythrocytes relative to the upper limits of normal ranges. Moreover, there was a significant decrease of the CAT level in blood plasma relative to the upper limits of normal ranges.

CONCLUSION: Thus, the results of the present study permit us to draw the following conclusions. The patients with psychotropic and NSAIDs drug-induced nephropathy have increased level of oxidative stress products and increased neutrophil gelatinase-associated lipocalin level even in normal eGFR. The mechanisms that lead to the development of oxidative stress and the production of modified proteins are different in patients treated with different drugs.

Downloads

Download data is not yet available.

Metrics

Metrics Loading ...

Plum Analytics Artifact Widget Block

References

Ghane Shahrbaf F, Assadi F. Drug-induced renal disorders. J Renal Inj Prev. 2015;4(3):57-60. PMid:26468475

Kim SY, Moon A. Drug-induced nephrotoxicity and its biomarkers. Biomol Ther (Seoul). 2012;20(3):268-72. PMid:24130922

Sales GT, Foresto RD. Drug-induced nephrotoxicity. Rev Assoc Med Bras (1922). 2020;66(1):82-90. PMid:31939540

Ungprasert P, Cheungpasitporn W, Crowson CS, Matteson EL. Individual non-steroidal anti-inflammatory drugs and risk of acute kidney injury: A systematic review and meta-analysis of observational studies. Eur J Intern Med. 2015;26(4):285-91. https://doi.org/10.1016/j.ejim.2015.03.008 PMid:25862494

Correll CU, Detraux J, De Lepeleire J, De Hert M. Effects of antipsychotics, antidepressants and mood stabilizers on risk for physical diseases in people with schizophrenia, depression and bipolar disorder. World Psychiatry. 2015;14(2):119-36. https:// doi.org/10.1002/wps.20204 PMid:26043321

Jiang Y, McCombs JS, Park SH. A retrospective cohort study of acute kidney injury risk associated with antipsychotics. CNS Drugs. 2017;31(4):319-26. https://doi.org/10.1007/ s40263-017-0421-4 PMid:28290080

Cordero MD, Sanchez-Alcazar JA, Bautista-Ferrufino MR, Carmona-López MI, Illanes M, Ríos MJ, et al. Acute oxidant damage promoted on cancer cells by amitriptyline in comparison with some common chemotherapeutic drugs. Anticancer Drugs. 2010;21(10):932-44. https://doi.org/10.1097/ cad.0b013e32833ed5f7 PMid:20847644

Hroudova J, Fisar Z. In vitro inhibition of mitochondrial respiratory rate by antidepressants. Toxicol Lett. 2012;213(3):345-52. https://doi.org/10.1016/j.toxlet.2012.07.017 PMid:22842584

Taziki S, Sattari MR, Dastmalchi S, Eghbal MA. Cytoprotective effects of melatonin against amitriptyline-induced toxicity in isolated rat hepatocytes. Adv Pharm Bull. 2015;5(3):329-34. https://doi.org/10.15171/apb.2015.046 PMid:26504754

Muravlyova LE, Molotov-Luchanskiy VB, Kolesnikova YA. The modified proteins in erythrocytes and regulation of erythrocytes volume in patients with chronic kidney disease. Eur Rev Med Pharmacol Sci. 2015;19(22):4270-4. https://doi.org/10.1016/j. freeradbiomed.2014.10.775 PMid:26636513

Piwowar A. Advanced oxidation protein products. Part I. Mechanism of the formation, characteristics and property. Pol Merkur Lekarski. 2010;28(164):166-9. PMid:20369749

Rabbani N, Thornalley PJ Advanced glycation end products in the pathogenesis of chronic kidney disease. Kidney Int. 2018;93(4):803-13. https://doi.org/10.1016/j.kint.2017.11.034 PMid:29477239

Husna AH, Ramadhani EA, Eva DT, Yulita AF, Suhartono E. The role formation of methylglyoxal, carbonyl compound, hydrogen peroxide and advance oxidation protein product induced cadmium in ovarian rat. Int J Chem Eng Appl. 2014;5(4):319-23. https://doi.org/10.7763/ijcea.2014.v5.402

Crawford A, Fasett RG, Coombes JS, Kunde DA, Ahuja KD, Robertson IK, et al. Glutathione peroxidase, superoxide dismutase and catalase genotypes and activities and the progression of chronic kidney disease. Nephrol Dial Transplant. 2011;26(9):2806-13. https://doi.org/10.1093/ndt/gfq828 PMid:21325350

Griffin BR, Faubel S, Edelstein CL. Biomarkers of drug-induced kidney toxicity. Ther Drug Monit. 2019;41(2):213-26. https://doi. org/10.1097/ftd.0000000000000589 PMid:30883514

Stadtman ER, Levine RL. Protein oxidation. Ann N Y Acad Sci. 2000;899:191-208. PMid:10863540

Witko-Sarsat V, Frielander M, Capeillere-Blandin C, Nguyen- Khoa T, Nguyen AT, Zingraff J, et al. Advanced oxidation protein products as a novel marker of oxidative stress in uremia. Kidney Int. 1996;49:1304-13. https://doi.org/10.1038/ki.1996.186 PMid:8731095

Racker E, Colowick SP, Kaplan NO. Methods in Enzymology. Vol. 3. Cambridge: Academic Press; 1963. p. 283.

Korolyuk MA, Ivanova LI, Maĭorova IG, Tokarev VE. A method of determining catalase activity. Lab Delo. 1988;1:16-9. PMid:2451064

Aeby HE. Catalase in vitro. Methods Enzymol. 1984;105:121-6. PMid:6727660

McDonald JH. Handbook of Biological Statistics. 3rd ed. Baltimore, Maryland, USA: Sparky House Publishing; 2014. p. 146-8.

Downloads

Published

2020-04-26

How to Cite

1.
Lee V, Bakirova R, Muravlyova L, Turkhanova Z, Rakhmetova A. Drug-induced Nephropathy and Molecular Patterns of Oxidative Stress. Open Access Maced J Med Sci [Internet]. 2020 Apr. 26 [cited 2024 Apr. 24];8(B):205-9. Available from: https://oamjms.eu/index.php/mjms/article/view/3559

Most read articles by the same author(s)