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Ранние биомаркеры нефротоксичности анти-VEGF противоопухолевых препаратов
Ранние биомаркеры нефротоксичности анти-VEGF противоопухолевых препаратов
Гречухина К.С., Чеботарева Н.В., Жукова Л.Г., Андросова Т.В., Карпов В.В., Краснова Т.Н. Ранние биомаркеры нефротоксичности анти-VEGF противоопухолевых препаратов. Терапевтический архив. 2022;94(6):725–730. DOI: 10.26442/00403660.2022.06.201561
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Аннотация
Обоснование. Антиангиогенные препараты широко используются в онкологической практике и направлены на торможение ангиогенеза. Несмотря на высокую противоопухолевую эффективность, их применение может быть ограничено нефротоксичностью, в связи с чем актуальным остается поиск ранних биомаркеров повреждения почек, которые позволили бы сохранить благоприятный профиль безопасности терапии.
Цель. Определить мочевые биомаркеры тубулярного и подоцитарного повреждения почек у больных, получающих лечение антиангиогенными препаратами.
Материалы и методы. В исследование вошли пациенты (n=50), получавшие внутривенные анти-VEGF-препараты (афлиберцепт, бевацизумаб, рамуцирумаб) в различных схемах химиотерапии. Концентрации канальцевых маркеров повреждения KIM-1 (Kidney Injury Molecule-1) и NGAL (Neutrophil Gelatinase-Associated Lipocalin), а также маркера гипоксии HIF-1α (Hypoxia-Inducible Factor 1-alpha) в образцах мочи определяли методом иммуноферментного анализа до лечения и в течение 8 нед терапии. Для оценки факторов риска повреждения почек проводили логистический регрессионный анализ с включением основных клинико-лабораторных показателей.
Результаты. Снижение расчетной скорости клубочковой фильтрации по формуле CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration Formula) <60 мл/мин на 1,73 м2 на 8-й неделе лечения отмечено у 42% больных. Повышение содержания NGAL, KIM-1, HIF-1α и нефрина в моче в течение первых 2 нед терапии прогнозировало развитие почечного повреждения к 8-й неделе наблюдения. При построении ROC-кривых установлена высокая чувствительность и специфичность этих мочевых показателей в качестве прогностических маркеров. Среди клинико-лабораторных показателей независимыми неблагоприятными прогностическими факторами нефротоксичности стали исходное снижение расчетной скорости клубочковой фильтрации, наличие в анамнезе артериальной гипертензии, нарастание концентрации в моче KIM-1 и HIF-1α в течение первых 2 нед терапии.
Заключение. Предиктором почечного повреждения при лечении антиангиогенными препаратами оказалось раннее повышение NGAL, KIM-1 и HIF-1α в моче в течение первых 2 нед от начала терапии.
Ключевые слова: повреждение почек, антиангиогенная терапия, тромботическая микроангиопатия, ранние биомаркеры, KIM-1, NGAL, HIF-1α
Aim. To determine urinary biomarkers of tubular and podocyte damage in patients receiving treatment with antiangiogenic drugs.
Materials and methods. The study included patients (n=50) who received intravenous anti-VEGF drugs (aflibercept, bevacizumab, ramucirumab) in various chemotherapy regimens. Concentrations of tubular damage markers KIM-1 (Kidney Injury Molecule-1) and NGAL (Neutrophil Gelatinase-Associated Lipocalin), hypoxia marker HIF-1α (Hypoxia-Inducible Factor 1-alpha) in urine samples were determined by enzyme-linked immunosorbent assay (ELISA) before treatment, and during 8 weeks of treatment. To assess the risk factors for kidney damage, a logistic regression analysis was performed with the inclusion of the main clinical and laboratory parameters.
Results. A decrease in the calculated GFR of CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration Formula) of less than 60 ml/min per 1.73 m2 at week 8 of treatment was noted in 42% of patients. An increase in NGAL, KIM-1, HIF-1α and nephrin in urine during the first two weeks of therapy predicted the development of renal damage by the 8th week of follow-up. When constructing ROC-curves, the high sensitivity and specificity of these urinary indicators as prognostic markers were established. Among the clinical and laboratory indicators, independent unfavorable prognostic factors of nephrotoxicity were an initial decrease in eGFR, a history of hypertension, an increase in the concentration of KIM-1 and HIF-1α in urine during the first two weeks of therapy.
Conclusion. The predictors of renal damage in the treatment with antiangiogenic drugs were previously an increase in NGAL, KIM-1 and HIF-1α in urine during the first two weeks after the start of therapy.
Keywords: kidney injury, antiangiogenic therapy, thrombotic microangiopathy, early biomarkers, KIM-1, NGAL, HIF-1α
Цель. Определить мочевые биомаркеры тубулярного и подоцитарного повреждения почек у больных, получающих лечение антиангиогенными препаратами.
Материалы и методы. В исследование вошли пациенты (n=50), получавшие внутривенные анти-VEGF-препараты (афлиберцепт, бевацизумаб, рамуцирумаб) в различных схемах химиотерапии. Концентрации канальцевых маркеров повреждения KIM-1 (Kidney Injury Molecule-1) и NGAL (Neutrophil Gelatinase-Associated Lipocalin), а также маркера гипоксии HIF-1α (Hypoxia-Inducible Factor 1-alpha) в образцах мочи определяли методом иммуноферментного анализа до лечения и в течение 8 нед терапии. Для оценки факторов риска повреждения почек проводили логистический регрессионный анализ с включением основных клинико-лабораторных показателей.
Результаты. Снижение расчетной скорости клубочковой фильтрации по формуле CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration Formula) <60 мл/мин на 1,73 м2 на 8-й неделе лечения отмечено у 42% больных. Повышение содержания NGAL, KIM-1, HIF-1α и нефрина в моче в течение первых 2 нед терапии прогнозировало развитие почечного повреждения к 8-й неделе наблюдения. При построении ROC-кривых установлена высокая чувствительность и специфичность этих мочевых показателей в качестве прогностических маркеров. Среди клинико-лабораторных показателей независимыми неблагоприятными прогностическими факторами нефротоксичности стали исходное снижение расчетной скорости клубочковой фильтрации, наличие в анамнезе артериальной гипертензии, нарастание концентрации в моче KIM-1 и HIF-1α в течение первых 2 нед терапии.
Заключение. Предиктором почечного повреждения при лечении антиангиогенными препаратами оказалось раннее повышение NGAL, KIM-1 и HIF-1α в моче в течение первых 2 нед от начала терапии.
Ключевые слова: повреждение почек, антиангиогенная терапия, тромботическая микроангиопатия, ранние биомаркеры, KIM-1, NGAL, HIF-1α
________________________________________________
Aim. To determine urinary biomarkers of tubular and podocyte damage in patients receiving treatment with antiangiogenic drugs.
Materials and methods. The study included patients (n=50) who received intravenous anti-VEGF drugs (aflibercept, bevacizumab, ramucirumab) in various chemotherapy regimens. Concentrations of tubular damage markers KIM-1 (Kidney Injury Molecule-1) and NGAL (Neutrophil Gelatinase-Associated Lipocalin), hypoxia marker HIF-1α (Hypoxia-Inducible Factor 1-alpha) in urine samples were determined by enzyme-linked immunosorbent assay (ELISA) before treatment, and during 8 weeks of treatment. To assess the risk factors for kidney damage, a logistic regression analysis was performed with the inclusion of the main clinical and laboratory parameters.
Results. A decrease in the calculated GFR of CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration Formula) of less than 60 ml/min per 1.73 m2 at week 8 of treatment was noted in 42% of patients. An increase in NGAL, KIM-1, HIF-1α and nephrin in urine during the first two weeks of therapy predicted the development of renal damage by the 8th week of follow-up. When constructing ROC-curves, the high sensitivity and specificity of these urinary indicators as prognostic markers were established. Among the clinical and laboratory indicators, independent unfavorable prognostic factors of nephrotoxicity were an initial decrease in eGFR, a history of hypertension, an increase in the concentration of KIM-1 and HIF-1α in urine during the first two weeks of therapy.
Conclusion. The predictors of renal damage in the treatment with antiangiogenic drugs were previously an increase in NGAL, KIM-1 and HIF-1α in urine during the first two weeks after the start of therapy.
Keywords: kidney injury, antiangiogenic therapy, thrombotic microangiopathy, early biomarkers, KIM-1, NGAL, HIF-1α
Полный текст
Список литературы
1. Ferrara N, Gerber H, LeCouter J. The biology of VEGF and its receptors. Nat Med. 2003;9(6):669-76. DOI:10.1038/nm0603-669
2. Zirlik K, Duyster J. Anti-Angiogenics: Current Situation and Future Perspectives. Oncol Res Treat. 2018;41(4):166-17. DOI:10.1159/000488087
3. Pastorino A, Di Bartolomeo M, Maiello E, et al. Aflibercept Plus FOLFIRI in the Real-life Setting: Safety and Quality of Life Data From the Italian Patient Cohort of the Aflibercept Safety and Quality-of-Life Program Study. Clin Colorectal Cancer. 2018;17(3):e457-70. DOI:10.1016/j.clcc.2018.03.002
4. Giantonio BJ, Catalano PJ, Meropol NJ, et al. Bevacizumab in Combination With Oxaliplatin, Fluorouracil, and Leucovorin (FOLFOX4) for Previously Treated Metastatic Colorectal Cancer: Results From the Eastern Cooperative Oncology Group Study E3200. J Clin Oncol. 2007;25(12):1539-44. DOI:10.1200/JCO.2006.09.6305
5. Wang Z, Dabrosin C, Yin X, et al. Broad targeting of angiogenesis for cancer prevention and therapy. Semin Cancer Biol. 2015;35(Suppl.):S224-43. DOI:10.1016/j.semcancer.2015.01.001
6. Mourad JJ, des Guetz G, Debbabi H, Levy BI. Blood pressure rise following angiogenesis inhibition by bevacizumab. A crucial role for microcirculation. Ann Oncol. 2008;19(5):927-34. DOI:10.1093/annonc/mdm550
7. Qi WX, Shen Z, Tang LN, Yao Y. Risk of Hypertension in Cancer Patients Treated with Aflibercept: A Systematic Review and Meta-Analysis. Clin Drug Investig. 2014;34(4):231-40. DOI:10.1007/s40261-014-0174-5
8. Touyz R, Herrmann S, Herrmann J. Vascular toxicities with VEGF inhibitor therapies – focus on hypertension and arterial thrombotic events. J Am Soc Hypertens. 2018;12(6):409-25. DOI:10.1016/j.jash.2018.03.008
9. Toriu A, Sekine A, Mizuno H, et al. Renal-Limited Thrombotic Microangiopathy due to Bevacizumab Therapy for Metastatic Colorectal Cancer: A Case Report. Case Rep Oncol. 2019;12(2):391-400. DOI:10.1159/000500716
10. Piscitani L, Sirolli V, Di Liberato L, et al. Nephrotoxicity Associated with Novel Anticancer Agents (Aflibercept, Dasatinib, Nivolumab): Case Series and Nephrological Considerations. Int J Mol Sci. 2020;21(14):4878. DOI:10.3390/ijms21144878
11. Hanna RM, Tran NT, Patel SS, et al. Thrombotic Microangiopathy and Acute Kidney Injury Induced After Intravitreal Injection of Vascular Endothelial Growth Factor Inhibitors VEGF Blockade-Related TMA After Intravitreal Use. Front Med (Lausanne). 2020;7:579603. DOI:10.3389/fmed.2020.579603
12. Morales E, Moliz C, Gutierrez E. Renal damage associated to intravitreal administration of ranibizumab. Nefrologia. 2017;37(6):653‑5. DOI:10.1016/j.nefro.2016.10.011
13. Florova B, Rajdl D, Racek J, et al. NGAL, albumin and cystatin C during cisplatin therapy. Physiol Res. 2020;69(2):307-17. DOI:10.33549/physiolres.934212
14. Vaidya VS, Ford GM, Waikar SS, et al. A rapid urine test for early detection of kidney injury. Kidney Int. 2009;76(1):108-14. DOI:10.1038/ki.2009.96
15. Vaidya VS, Ozer JS, Dieterle F, et al. Kidney Injury Molecule-1 Outperforms Traditional Biomarkers of Kidney Injury in Multi-site Preclinical Biomarker Qualification Studies. Nat Biotechnol. 2010;28(5):478-85. DOI:10.1038/nbt.1623
16. Ghadrdan E, Ebrahimpour S, Sadighi S, et al. Evaluation of urinary neutrophil gelatinase-associated lipocalin and urinary kidney injury molecule-1 as biomarkers of renal function in cancer patients treated with cisplatin. J Oncol Pharm Pract. 2020;26(7):1643-9. DOI:10.1177/1078155220901756
17. Shu S, Wang Y, Zheng M, et al. Hypoxia and Hypoxia-Inducible Factors in Kidney Injury and Repair. Cells. 2019;3(8):207. DOI:10.3390/cells8030207
18. Ma C, Wei J, Zhan F, et al. Urinary hypoxia-inducible factor-1alpha levels are associated with histologic chronicity changes and renal function in patients with lupus nephritis. Yonsei Med J. 2012;53(3):587‑92. DOI:10.3349/ymj.2012.53.3.587
19. Niu G, Chen X. Vascular Endothelial Growth Factor as an Anti-angiogenic Target for Cancer Therapy. Curr Drug Targets. 2010;11(8):1000-17. DOI:10.2174/138945010791591395
20. Kazazi-Hyseni F, Beijnen J, Schellens J. Bevacizumab. Oncologist. 2010;15(8):819-25. DOI:10.1634/theoncologist.2009-0317
21. Maitland ML, Bakris GL, Black HR, et al. Initial assessment, surveillance, and management of blood pressure in patients receiving vascular endothelial growth factor signaling pathway inhibitors. J Natl Cancer Inst. 2010;102(9):596-604. DOI:10.1093/jnci/djq091
22. Steeghs N, Hovens MM, Rabelink AJ, et al. VEGF-R2 blockade in patients with solid tumors: mechanisms of hypertension and effects on vascular function. J Clin Oncol. 2006;18(Suppl.):3037. DOI:10.1200/jco.2006.24.18_suppl.3037
23. Hayman SR, Leung N, Grande JP, Garovic VD. VEGF inhibition, hypertension, and renal toxicity. Curr Oncol Rep. 2012;14(4):285-94. DOI:10.1007/s11912-012-0242-z
24. Bollee G, Patey N, Cazajous G, et al. Thrombotic microangiopathy secondary to VEGF pathway inhibition by sunitinib. Nephrol Dial Transplant. 2009;24(2):682-5. DOI:10.1093/ndt/gfn657
25. Hauser PV, Collino F, Bussolati B, Camussi G. Nephrin and endothelial injury. Curr Opin Nephrol Hypertens. 2009;18(1):3-8. DOI:10.1097/MNH.0b013e32831a4713
2. Zirlik K, Duyster J. Anti-Angiogenics: Current Situation and Future Perspectives. Oncol Res Treat. 2018;41(4):166-17. DOI:10.1159/000488087
3. Pastorino A, Di Bartolomeo M, Maiello E, et al. Aflibercept Plus FOLFIRI in the Real-life Setting: Safety and Quality of Life Data From the Italian Patient Cohort of the Aflibercept Safety and Quality-of-Life Program Study. Clin Colorectal Cancer. 2018;17(3):e457-70. DOI:10.1016/j.clcc.2018.03.002
4. Giantonio BJ, Catalano PJ, Meropol NJ, et al. Bevacizumab in Combination With Oxaliplatin, Fluorouracil, and Leucovorin (FOLFOX4) for Previously Treated Metastatic Colorectal Cancer: Results From the Eastern Cooperative Oncology Group Study E3200. J Clin Oncol. 2007;25(12):1539-44. DOI:10.1200/JCO.2006.09.6305
5. Wang Z, Dabrosin C, Yin X, et al. Broad targeting of angiogenesis for cancer prevention and therapy. Semin Cancer Biol. 2015;35(Suppl.):S224-43. DOI:10.1016/j.semcancer.2015.01.001
6. Mourad JJ, des Guetz G, Debbabi H, Levy BI. Blood pressure rise following angiogenesis inhibition by bevacizumab. A crucial role for microcirculation. Ann Oncol. 2008;19(5):927-34. DOI:10.1093/annonc/mdm550
7. Qi WX, Shen Z, Tang LN, Yao Y. Risk of Hypertension in Cancer Patients Treated with Aflibercept: A Systematic Review and Meta-Analysis. Clin Drug Investig. 2014;34(4):231-40. DOI:10.1007/s40261-014-0174-5
8. Touyz R, Herrmann S, Herrmann J. Vascular toxicities with VEGF inhibitor therapies – focus on hypertension and arterial thrombotic events. J Am Soc Hypertens. 2018;12(6):409-25. DOI:10.1016/j.jash.2018.03.008
9. Toriu A, Sekine A, Mizuno H, et al. Renal-Limited Thrombotic Microangiopathy due to Bevacizumab Therapy for Metastatic Colorectal Cancer: A Case Report. Case Rep Oncol. 2019;12(2):391-400. DOI:10.1159/000500716
10. Piscitani L, Sirolli V, Di Liberato L, et al. Nephrotoxicity Associated with Novel Anticancer Agents (Aflibercept, Dasatinib, Nivolumab): Case Series and Nephrological Considerations. Int J Mol Sci. 2020;21(14):4878. DOI:10.3390/ijms21144878
11. Hanna RM, Tran NT, Patel SS, et al. Thrombotic Microangiopathy and Acute Kidney Injury Induced After Intravitreal Injection of Vascular Endothelial Growth Factor Inhibitors VEGF Blockade-Related TMA After Intravitreal Use. Front Med (Lausanne). 2020;7:579603. DOI:10.3389/fmed.2020.579603
12. Morales E, Moliz C, Gutierrez E. Renal damage associated to intravitreal administration of ranibizumab. Nefrologia. 2017;37(6):653‑5. DOI:10.1016/j.nefro.2016.10.011
13. Florova B, Rajdl D, Racek J, et al. NGAL, albumin and cystatin C during cisplatin therapy. Physiol Res. 2020;69(2):307-17. DOI:10.33549/physiolres.934212
14. Vaidya VS, Ford GM, Waikar SS, et al. A rapid urine test for early detection of kidney injury. Kidney Int. 2009;76(1):108-14. DOI:10.1038/ki.2009.96
15. Vaidya VS, Ozer JS, Dieterle F, et al. Kidney Injury Molecule-1 Outperforms Traditional Biomarkers of Kidney Injury in Multi-site Preclinical Biomarker Qualification Studies. Nat Biotechnol. 2010;28(5):478-85. DOI:10.1038/nbt.1623
16. Ghadrdan E, Ebrahimpour S, Sadighi S, et al. Evaluation of urinary neutrophil gelatinase-associated lipocalin and urinary kidney injury molecule-1 as biomarkers of renal function in cancer patients treated with cisplatin. J Oncol Pharm Pract. 2020;26(7):1643-9. DOI:10.1177/1078155220901756
17. Shu S, Wang Y, Zheng M, et al. Hypoxia and Hypoxia-Inducible Factors in Kidney Injury and Repair. Cells. 2019;3(8):207. DOI:10.3390/cells8030207
18. Ma C, Wei J, Zhan F, et al. Urinary hypoxia-inducible factor-1alpha levels are associated with histologic chronicity changes and renal function in patients with lupus nephritis. Yonsei Med J. 2012;53(3):587‑92. DOI:10.3349/ymj.2012.53.3.587
19. Niu G, Chen X. Vascular Endothelial Growth Factor as an Anti-angiogenic Target for Cancer Therapy. Curr Drug Targets. 2010;11(8):1000-17. DOI:10.2174/138945010791591395
20. Kazazi-Hyseni F, Beijnen J, Schellens J. Bevacizumab. Oncologist. 2010;15(8):819-25. DOI:10.1634/theoncologist.2009-0317
21. Maitland ML, Bakris GL, Black HR, et al. Initial assessment, surveillance, and management of blood pressure in patients receiving vascular endothelial growth factor signaling pathway inhibitors. J Natl Cancer Inst. 2010;102(9):596-604. DOI:10.1093/jnci/djq091
22. Steeghs N, Hovens MM, Rabelink AJ, et al. VEGF-R2 blockade in patients with solid tumors: mechanisms of hypertension and effects on vascular function. J Clin Oncol. 2006;18(Suppl.):3037. DOI:10.1200/jco.2006.24.18_suppl.3037
23. Hayman SR, Leung N, Grande JP, Garovic VD. VEGF inhibition, hypertension, and renal toxicity. Curr Oncol Rep. 2012;14(4):285-94. DOI:10.1007/s11912-012-0242-z
24. Bollee G, Patey N, Cazajous G, et al. Thrombotic microangiopathy secondary to VEGF pathway inhibition by sunitinib. Nephrol Dial Transplant. 2009;24(2):682-5. DOI:10.1093/ndt/gfn657
25. Hauser PV, Collino F, Bussolati B, Camussi G. Nephrin and endothelial injury. Curr Opin Nephrol Hypertens. 2009;18(1):3-8. DOI:10.1097/MNH.0b013e32831a4713
2. Zirlik K, Duyster J. Anti-Angiogenics: Current Situation and Future Perspectives. Oncol Res Treat. 2018;41(4):166-17. DOI:10.1159/000488087
3. Pastorino A, Di Bartolomeo M, Maiello E, et al. Aflibercept Plus FOLFIRI in the Real-life Setting: Safety and Quality of Life Data From the Italian Patient Cohort of the Aflibercept Safety and Quality-of-Life Program Study. Clin Colorectal Cancer. 2018;17(3):e457-70. DOI:10.1016/j.clcc.2018.03.002
4. Giantonio BJ, Catalano PJ, Meropol NJ, et al. Bevacizumab in Combination With Oxaliplatin, Fluorouracil, and Leucovorin (FOLFOX4) for Previously Treated Metastatic Colorectal Cancer: Results From the Eastern Cooperative Oncology Group Study E3200. J Clin Oncol. 2007;25(12):1539-44. DOI:10.1200/JCO.2006.09.6305
5. Wang Z, Dabrosin C, Yin X, et al. Broad targeting of angiogenesis for cancer prevention and therapy. Semin Cancer Biol. 2015;35(Suppl.):S224-43. DOI:10.1016/j.semcancer.2015.01.001
6. Mourad JJ, des Guetz G, Debbabi H, Levy BI. Blood pressure rise following angiogenesis inhibition by bevacizumab. A crucial role for microcirculation. Ann Oncol. 2008;19(5):927-34. DOI:10.1093/annonc/mdm550
7. Qi WX, Shen Z, Tang LN, Yao Y. Risk of Hypertension in Cancer Patients Treated with Aflibercept: A Systematic Review and Meta-Analysis. Clin Drug Investig. 2014;34(4):231-40. DOI:10.1007/s40261-014-0174-5
8. Touyz R, Herrmann S, Herrmann J. Vascular toxicities with VEGF inhibitor therapies – focus on hypertension and arterial thrombotic events. J Am Soc Hypertens. 2018;12(6):409-25. DOI:10.1016/j.jash.2018.03.008
9. Toriu A, Sekine A, Mizuno H, et al. Renal-Limited Thrombotic Microangiopathy due to Bevacizumab Therapy for Metastatic Colorectal Cancer: A Case Report. Case Rep Oncol. 2019;12(2):391-400. DOI:10.1159/000500716
10. Piscitani L, Sirolli V, Di Liberato L, et al. Nephrotoxicity Associated with Novel Anticancer Agents (Aflibercept, Dasatinib, Nivolumab): Case Series and Nephrological Considerations. Int J Mol Sci. 2020;21(14):4878. DOI:10.3390/ijms21144878
11. Hanna RM, Tran NT, Patel SS, et al. Thrombotic Microangiopathy and Acute Kidney Injury Induced After Intravitreal Injection of Vascular Endothelial Growth Factor Inhibitors VEGF Blockade-Related TMA After Intravitreal Use. Front Med (Lausanne). 2020;7:579603. DOI:10.3389/fmed.2020.579603
12. Morales E, Moliz C, Gutierrez E. Renal damage associated to intravitreal administration of ranibizumab. Nefrologia. 2017;37(6):653‑5. DOI:10.1016/j.nefro.2016.10.011
13. Florova B, Rajdl D, Racek J, et al. NGAL, albumin and cystatin C during cisplatin therapy. Physiol Res. 2020;69(2):307-17. DOI:10.33549/physiolres.934212
14. Vaidya VS, Ford GM, Waikar SS, et al. A rapid urine test for early detection of kidney injury. Kidney Int. 2009;76(1):108-14. DOI:10.1038/ki.2009.96
15. Vaidya VS, Ozer JS, Dieterle F, et al. Kidney Injury Molecule-1 Outperforms Traditional Biomarkers of Kidney Injury in Multi-site Preclinical Biomarker Qualification Studies. Nat Biotechnol. 2010;28(5):478-85. DOI:10.1038/nbt.1623
16. Ghadrdan E, Ebrahimpour S, Sadighi S, et al. Evaluation of urinary neutrophil gelatinase-associated lipocalin and urinary kidney injury molecule-1 as biomarkers of renal function in cancer patients treated with cisplatin. J Oncol Pharm Pract. 2020;26(7):1643-9. DOI:10.1177/1078155220901756
17. Shu S, Wang Y, Zheng M, et al. Hypoxia and Hypoxia-Inducible Factors in Kidney Injury and Repair. Cells. 2019;3(8):207. DOI:10.3390/cells8030207
18. Ma C, Wei J, Zhan F, et al. Urinary hypoxia-inducible factor-1alpha levels are associated with histologic chronicity changes and renal function in patients with lupus nephritis. Yonsei Med J. 2012;53(3):587‑92. DOI:10.3349/ymj.2012.53.3.587
19. Niu G, Chen X. Vascular Endothelial Growth Factor as an Anti-angiogenic Target for Cancer Therapy. Curr Drug Targets. 2010;11(8):1000-17. DOI:10.2174/138945010791591395
20. Kazazi-Hyseni F, Beijnen J, Schellens J. Bevacizumab. Oncologist. 2010;15(8):819-25. DOI:10.1634/theoncologist.2009-0317
21. Maitland ML, Bakris GL, Black HR, et al. Initial assessment, surveillance, and management of blood pressure in patients receiving vascular endothelial growth factor signaling pathway inhibitors. J Natl Cancer Inst. 2010;102(9):596-604. DOI:10.1093/jnci/djq091
22. Steeghs N, Hovens MM, Rabelink AJ, et al. VEGF-R2 blockade in patients with solid tumors: mechanisms of hypertension and effects on vascular function. J Clin Oncol. 2006;18(Suppl.):3037. DOI:10.1200/jco.2006.24.18_suppl.3037
23. Hayman SR, Leung N, Grande JP, Garovic VD. VEGF inhibition, hypertension, and renal toxicity. Curr Oncol Rep. 2012;14(4):285-94. DOI:10.1007/s11912-012-0242-z
24. Bollee G, Patey N, Cazajous G, et al. Thrombotic microangiopathy secondary to VEGF pathway inhibition by sunitinib. Nephrol Dial Transplant. 2009;24(2):682-5. DOI:10.1093/ndt/gfn657
25. Hauser PV, Collino F, Bussolati B, Camussi G. Nephrin and endothelial injury. Curr Opin Nephrol Hypertens. 2009;18(1):3-8. DOI:10.1097/MNH.0b013e32831a4713
________________________________________________
2. Zirlik K, Duyster J. Anti-Angiogenics: Current Situation and Future Perspectives. Oncol Res Treat. 2018;41(4):166-17. DOI:10.1159/000488087
3. Pastorino A, Di Bartolomeo M, Maiello E, et al. Aflibercept Plus FOLFIRI in the Real-life Setting: Safety and Quality of Life Data From the Italian Patient Cohort of the Aflibercept Safety and Quality-of-Life Program Study. Clin Colorectal Cancer. 2018;17(3):e457-70. DOI:10.1016/j.clcc.2018.03.002
4. Giantonio BJ, Catalano PJ, Meropol NJ, et al. Bevacizumab in Combination With Oxaliplatin, Fluorouracil, and Leucovorin (FOLFOX4) for Previously Treated Metastatic Colorectal Cancer: Results From the Eastern Cooperative Oncology Group Study E3200. J Clin Oncol. 2007;25(12):1539-44. DOI:10.1200/JCO.2006.09.6305
5. Wang Z, Dabrosin C, Yin X, et al. Broad targeting of angiogenesis for cancer prevention and therapy. Semin Cancer Biol. 2015;35(Suppl.):S224-43. DOI:10.1016/j.semcancer.2015.01.001
6. Mourad JJ, des Guetz G, Debbabi H, Levy BI. Blood pressure rise following angiogenesis inhibition by bevacizumab. A crucial role for microcirculation. Ann Oncol. 2008;19(5):927-34. DOI:10.1093/annonc/mdm550
7. Qi WX, Shen Z, Tang LN, Yao Y. Risk of Hypertension in Cancer Patients Treated with Aflibercept: A Systematic Review and Meta-Analysis. Clin Drug Investig. 2014;34(4):231-40. DOI:10.1007/s40261-014-0174-5
8. Touyz R, Herrmann S, Herrmann J. Vascular toxicities with VEGF inhibitor therapies – focus on hypertension and arterial thrombotic events. J Am Soc Hypertens. 2018;12(6):409-25. DOI:10.1016/j.jash.2018.03.008
9. Toriu A, Sekine A, Mizuno H, et al. Renal-Limited Thrombotic Microangiopathy due to Bevacizumab Therapy for Metastatic Colorectal Cancer: A Case Report. Case Rep Oncol. 2019;12(2):391-400. DOI:10.1159/000500716
10. Piscitani L, Sirolli V, Di Liberato L, et al. Nephrotoxicity Associated with Novel Anticancer Agents (Aflibercept, Dasatinib, Nivolumab): Case Series and Nephrological Considerations. Int J Mol Sci. 2020;21(14):4878. DOI:10.3390/ijms21144878
11. Hanna RM, Tran NT, Patel SS, et al. Thrombotic Microangiopathy and Acute Kidney Injury Induced After Intravitreal Injection of Vascular Endothelial Growth Factor Inhibitors VEGF Blockade-Related TMA After Intravitreal Use. Front Med (Lausanne). 2020;7:579603. DOI:10.3389/fmed.2020.579603
12. Morales E, Moliz C, Gutierrez E. Renal damage associated to intravitreal administration of ranibizumab. Nefrologia. 2017;37(6):653‑5. DOI:10.1016/j.nefro.2016.10.011
13. Florova B, Rajdl D, Racek J, et al. NGAL, albumin and cystatin C during cisplatin therapy. Physiol Res. 2020;69(2):307-17. DOI:10.33549/physiolres.934212
14. Vaidya VS, Ford GM, Waikar SS, et al. A rapid urine test for early detection of kidney injury. Kidney Int. 2009;76(1):108-14. DOI:10.1038/ki.2009.96
15. Vaidya VS, Ozer JS, Dieterle F, et al. Kidney Injury Molecule-1 Outperforms Traditional Biomarkers of Kidney Injury in Multi-site Preclinical Biomarker Qualification Studies. Nat Biotechnol. 2010;28(5):478-85. DOI:10.1038/nbt.1623
16. Ghadrdan E, Ebrahimpour S, Sadighi S, et al. Evaluation of urinary neutrophil gelatinase-associated lipocalin and urinary kidney injury molecule-1 as biomarkers of renal function in cancer patients treated with cisplatin. J Oncol Pharm Pract. 2020;26(7):1643-9. DOI:10.1177/1078155220901756
17. Shu S, Wang Y, Zheng M, et al. Hypoxia and Hypoxia-Inducible Factors in Kidney Injury and Repair. Cells. 2019;3(8):207. DOI:10.3390/cells8030207
18. Ma C, Wei J, Zhan F, et al. Urinary hypoxia-inducible factor-1alpha levels are associated with histologic chronicity changes and renal function in patients with lupus nephritis. Yonsei Med J. 2012;53(3):587‑92. DOI:10.3349/ymj.2012.53.3.587
19. Niu G, Chen X. Vascular Endothelial Growth Factor as an Anti-angiogenic Target for Cancer Therapy. Curr Drug Targets. 2010;11(8):1000-17. DOI:10.2174/138945010791591395
20. Kazazi-Hyseni F, Beijnen J, Schellens J. Bevacizumab. Oncologist. 2010;15(8):819-25. DOI:10.1634/theoncologist.2009-0317
21. Maitland ML, Bakris GL, Black HR, et al. Initial assessment, surveillance, and management of blood pressure in patients receiving vascular endothelial growth factor signaling pathway inhibitors. J Natl Cancer Inst. 2010;102(9):596-604. DOI:10.1093/jnci/djq091
22. Steeghs N, Hovens MM, Rabelink AJ, et al. VEGF-R2 blockade in patients with solid tumors: mechanisms of hypertension and effects on vascular function. J Clin Oncol. 2006;18(Suppl.):3037. DOI:10.1200/jco.2006.24.18_suppl.3037
23. Hayman SR, Leung N, Grande JP, Garovic VD. VEGF inhibition, hypertension, and renal toxicity. Curr Oncol Rep. 2012;14(4):285-94. DOI:10.1007/s11912-012-0242-z
24. Bollee G, Patey N, Cazajous G, et al. Thrombotic microangiopathy secondary to VEGF pathway inhibition by sunitinib. Nephrol Dial Transplant. 2009;24(2):682-5. DOI:10.1093/ndt/gfn657
25. Hauser PV, Collino F, Bussolati B, Camussi G. Nephrin and endothelial injury. Curr Opin Nephrol Hypertens. 2009;18(1):3-8. DOI:10.1097/MNH.0b013e32831a4713
Авторы
К.С. Гречухина*1,2, Н.В. Чеботарева1,3, Л.Г. Жукова2, Т.В. Андросова3, В.В. Карпов3, Т.Н. Краснова1,3
1 ФГБОУ ВО «Московский государственный университет им. М.В. Ломоносова», Москва, Россия;
2 ГБУЗ «Московский клинический научно-практический центр им. А.С. Логинова» Департамента здравоохранения г. Москвы, Москва, Россия;
3 ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет), Москва, Россия
*dr.grechukhina@gmail.com
1 Lomonosov Moscow State University, Moscow, Russia;
2 Loginov Moscow Clinical Scientific Center, Moscow, Russia;
3 Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia
*dr.grechukhina@gmail.com
1 ФГБОУ ВО «Московский государственный университет им. М.В. Ломоносова», Москва, Россия;
2 ГБУЗ «Московский клинический научно-практический центр им. А.С. Логинова» Департамента здравоохранения г. Москвы, Москва, Россия;
3 ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет), Москва, Россия
*dr.grechukhina@gmail.com
________________________________________________
1 Lomonosov Moscow State University, Moscow, Russia;
2 Loginov Moscow Clinical Scientific Center, Moscow, Russia;
3 Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia
*dr.grechukhina@gmail.com
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