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Abstract
Cisplatin has been used extensively as a cancer treatment. Nephrotoxicity, which is assessed by blood urea levels, blood creatinine, and estimated glomerular filtration rate (eGFR), is caused by cisplatin metabolites that build up in the kidneys. Because of these indicators' numerous flaws, optimal biological markers are required. One of the key mediators of inflammatory processes, such as kidney fibrosis and inflammation, is periostin. In cancer patients undergoing high-dose cisplatin therapy, the purpose of this study is to ascertain how urine periostin changes and how it relates to kidney function. This cross-sectional study was carried out at the National Center General Hospital of Cipto Mangunkusumo's medical hematology-oncology outer clinic and medical hematology-oncology ward on the eighth floor starting in November 2019 and ending when the minimum sample was obtained through consecutive sampling. Data was analyzed by IBM SPSS Statistics for Windows version 23.0 based on the research objective. Of the 37 responders, 70.3% were men, 29.7% were between the ages of 41 and 50, 78.4% were married, 59.5% had completed high school, 37.8% were employed, 59.5% had NPC, and 64.9% had a Karnofsky score of 80. Between before and one week following chemotherapy II, the respondents' blood creatinine and urea levels rose. The eGFR value has also decreased. Periostin levels, on the other hand, tended to rise one week following treatment III after declining during chemotherapy I and II (p value>0.05). Urine periostin levels and other kidney function indicators did not significantly correlate (p>0.05), according to the correlation test, and several domains had negative directions. The correlation coefficient values were modest (r = 0.017-0.254). There is a changing of urine periostin level of malignant patients receiving high dose cisplatin therapy which increase after the third chemotherapy. No significant correlation was found between periostin levels and kidney function in malignant patients with high-dose cisplatin therapy.
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References
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References
Aldossary, S. A. (2019). Review on pharmacology of cisplatin: Clinical use, toxicity and mechanism of resistance of cisplatin. Biomedical and Pharmacology Journal, 12(1), 7–15. https://doi.org/10.13005/bpj/1608
An, J. N., Yang, S. H., Kim, Y. C., Hwang, J. H., Park, J. Y., Kim, D. K., Kim, J. H., Kim, D. W., Hur, D. G., Oh, Y. K., Lim, C. S., Kim, Y. S., & Lee, J. P. (2019). Periostin induces kidney fibrosis after acute kidney injury via the p38 MAPK pathway. American Journal of Physiology-Renal Physiology, 316(3), F426–F437. https://doi.org/10.1152/ajprenal.00203.2018
Ashley, S. L., Wilke, C. A., Kim, K. K., & Moore, B. B. (2017). Periostin regulates fibrocyte function to promote myofibroblast differentiation and lung fibrosis. Mucosal Immunology, 10(2), 341–351. https://doi.org/10.1038/mi.2016.61
Dasari, S., & Bernard Tchounwou, P. (2014). Cisplatin in cancer therapy: Molecular mechanisms of action. In European Journal of Pharmacology (Vol. 740, pp. 364–378). Elsevier. https://doi.org/10.1016/j.ejphar.2014.07.025
Djordjević, M., Ilić, J., & Stojanovic, N. M. (2023). CISPLATIN - AN OVERVIEW OF ITS EFFICIENCY AND TOXICITY. Facta Universitatis, Series: Medicine and Biology. https://doi.org/10.22190/fumb230122002d
Duan, X., Chen, C., Liu, X., Wang, T., Feng, S., Li, J., & Li, G. (2023). Interference of periostin attenuates pathological changes, proinflammatory markers and renal fibrosis in diabetic kidney injury. Genes & Genomics, 45(11), 1389–1397. https://doi.org/10.1007/s13258-023-01400-x
Fang, C. yan, Lou, D. yong, Zhou, L. qin, Wang, J. cheng, Yang, B., He, Q. jun, Wang, J. jia, & Weng, Q. jie. (2021). Natural products: potential treatments for cisplatin-induced nephrotoxicity. In Acta Pharmacologica Sinica (Vol. 42, Issue 12, pp. 1951–1969). Springer Nature. https://doi.org/10.1038/s41401-021-00620-9
IBM Corp. (2015). IBM SPSS Statistics for Windows, version 23.0. IBM Corp. https://www.ibm.com/products/spss-statistics
Jia, Y. yuan, Yu, Y., & Li, H. jun. (2020). The research status and prospect of Periostin in chronic kidney disease. In Renal Failure (Vol. 42, Issue 1, pp. 1166–1172). Taylor and Francis Ltd. https://doi.org/10.1080/0886022X.2020.1846562
Muglia, L., Di Dio, M., Filicetti, E., Greco, G. I., Volpentesta, M., Beccacece, A., Fabbietti, P., Lattanzio, F., Corsonello, A., Gembillo, G., Santoro, D., & Soraci, L. (2024). Biomarkers of chronic kidney disease in older individuals: navigating complexity in diagnosis. In Frontiers in Medicine (Vol. 11). Frontiers Media SA. https://doi.org/10.3389/fmed.2024.1397160
Ostermann, M., & Joannidis, M. (2016). Acute kidney injury 2016: Diagnosis and diagnostic workup. In Critical Care (Vol. 20, Issue 1). BioMed Central Ltd. https://doi.org/10.1186/s13054-016-1478-z
Ozkok, A., & Edelstein, C. L. (2014). Pathophysiology of cisplatin-induced acute kidney injury. In BioMed Research International (Vol. 2014). Hindawi Publishing Corporation. https://doi.org/10.1155/2014/967826
Pană, N., & Căpușă, C. (2022). Periostin as a Biomarker in the Setting of Glomerular Diseases—A Review of the Current Literature. In Biomedicines (Vol. 10, Issue 12). MDPI. https://doi.org/10.3390/biomedicines10123211
Prakoura, N., & Chatziantoniou, C. (2017). Periostin in kidney diseases. In Cellular and Molecular Life Sciences (Vol. 74, Issue 23, pp. 4315–4320). Birkhauser Verlag AG. https://doi.org/10.1007/s00018-017-2650-6
Prasaja, Y., Sutandyo, N., & Andrajati, R. (2015). Incidence of cisplatin-induced nephrotoxicity and associated factors among cancer patients in Indonesia. Asian Pacific Journal of Cancer Prevention, 16(3), 1117–1122. https://doi.org/10.7314/APJCP.2015.16.3.1117
Satirapoj, B. (2018). Tubulointerstitial Biomarkers for Diabetic Nephropathy. In Journal of Diabetes Research (Vol. 2018). Hindawi Limited. https://doi.org/10.1155/2018/2852398
Satirapoj, B., Tassanasorn, S., Charoenpitakchai, M., & Supasyndh, O. (2015). Periostin as a tissue and urinary biomarker of renal injury in type 2 diabetes mellitus. PLoS ONE, 10(4). https://doi.org/10.1371/journal.pone.0124055
Satirapoj, B., Witoon, R., Ruangkanchanasetr, P., Wantanasiri, P., Charoenpitakchai, M., & Choovichian, P. (2014). Urine Periostin as a Biomarker of Renal Injury in Chronic Allograft Nephropathy. Transplantation Proceedings, 46(1), 135–140. https://doi.org/10.1016/j.transproceed.2013.07.069
Sharp, C. N., & Siskind, L. J. (2017). Developing better mouse models to study cisplatin-induced kidney injury. American Journal of Physiology-Renal Physiology, 313(4), F835–F841. https://doi.org/10.1152/ajprenal.00285.2017
Turczyn, A., & Pańczyk-Tomaszewska, M. (2021). The role of periostin in kidney diseases. Central European Journal of Immunology, 46(4), 494–501. https://doi.org/10.5114/ceji.2021.110317
Watanabe, E. H., Amaral, A. G., & Onuchic, L. F. (2019). Periostin and polycystic kidney disease: more pieces in the puzzle. American Journal of Physiology-Renal Physiology, 316(1), F159–F161. https://doi.org/10.1152/ajprenal.00518.2018
Yu, J.-B., Padanilam, B. J., & Kim, J. (2024). Activation of Yes-Associated Protein Is Indispensable for Transformation of Kidney Fibroblasts into Myofibroblasts during Repeated Administration of Cisplatin. Cells, 13(17), 1475. https://doi.org/10.3390/cells13171475
Zahedi, K., Barone, S., Brooks, M., Stewart, T. M., Foley, J. R., Nwafor, A., Casero, R. A., & Soleimani, M. (2024). Polyamine Catabolism and Its Role in Renal Injury and Fibrosis in Mice Subjected to Repeated Low-Dose Cisplatin Treatment. Biomedicines, 12(3), 640. https://doi.org/10.3390/biomedicines12030640
Zhu, S., Huo, L., Zeng, J., Chen, R., Sun, Y., Tan, M., Fan, M., Liu, M., Zhao, J., Huang, G., Wang, Y., Xiao, Z., & Zhao, Z. (2024). Differentiated management of ROS level in tumor and kidney to alleviate Cis-platinum induced acute kidney injury with improved efficacy. Journal of Nanobiotechnology, 22(1), 436. https://doi.org/10.1186/s12951-024-02710-2
Zyłka, A., Dumnicka, P., Kuśnierz-Cabala, B., Gala-Błądzińska, A., Ceranowicz, P., Kucharz, J., Ząbek-Adamska, A., Maziarz, B., Drozdz, R., & Kuźniewski, M. (2018). Markers of Glomerular and Tubular Damage in the Early Stage of Kidney Disease in Type 2 Diabetic Patients. Mediators of Inflammation, 2018. https://doi.org/10.1155/2018/7659243