Клинико-лабораторные признаки и факторы риска нефротоксичности антиангиогенных противоопухолевых препаратов - Журнал Терапевтический архив № 6 Вопросы нефрологии 2021
Клинико-лабораторные признаки и факторы риска нефротоксичности антиангиогенных противоопухолевых препаратов
Гречухина К.С., Чеботарева Н.В., Жукова Л.Г., Краснова Т.Н. Клинико-лабораторные признаки и факторы риска нефротоксичности антиангиогенных противоопухолевых препаратов. Терапевтический архив. 2021; 93 (6): 661–666. DOI: 10.26442/00403660.2021.06.200879
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Аннотация
Обоснование. Антиангиогенные противоопухолевые препараты, направленные на блокирование сигнального пути сосудистого эндотелиального фактора роста, могут вызывать различные нежелательные явления, среди которых почечное повреждение. Оценка риска нефротоксичности позволяет разработать оптимальные подходы к лечению и обеспечить относительную безопасность терапии.
Цель. Оценить ранние клинико-лабораторные проявления и факторы риска нефротоксичности антиангиогенных противоопухолевых препаратов.
Материалы и методы. В исследование вошли 50 пациентов, получавших антиангиогенные препараты в составе противоопухолевой химиотерапии. Оценивали демографические показатели, индекс массы тела, цифры артериального давления, тип антиангиогенного препарата, сопроводительную терапию. До начала лечения и в динамике в течение 8 нед с помощью критерия Фридмана оценивали уровень гемоглобина, тромбоцитов, шистоцитов, D-димера, лактатдегидрогеназы сыворотки крови, а также суточной протеинурии и креатинина сыворотки крови и расчетной скорости клубочковой фильтрации (СКФ) по CKD-EPI. Для оценки факторов риска нефротоксичности и артериальной гипертензии (АГ) проводили линейный регрессионный анализ.
Результаты. Медиана возраста пациентов составила 46 [34–57] лет, 22 (44%) мужчины и 28 (56%) женщин. АГ развилась у 52%, снижение СКФ – у 42% наряду со снижением гемоглобина и повышением лактатдегидрогеназы на 2-й неделе терапии. Число шистоцитов и тромбоцитов достоверно снизилось к 8-й неделе терапии. Факторами риска нарушения функции почек на фоне лечения антиангиогенными препаратами стали исходное снижение СКФ<80 мл/мин, повышение D-димера, уменьшение гемоглобина к 8-й неделе лечения. Факторами риска формирования АГ на фоне терапии оказались исходное снижение расчетной СКФ<80 мл/мин и отсутствие профилактической антикоагулянтной терапии.
Заключение. Ранними признаками нефротоксичности антиангиогенных противоопухолевых препаратов являлись снижение СКФ и развитие АГ. Независимыми факторами риска нефротоксичности стали исходное снижение СКФ, повышение D-димера и уменьшение гемоглобина на 8-й неделе лечения, в то же время профилактическое применение антикоагулянтной терапии снижало этот риск в нашем исследовании. Данные изменения можно рассматривать в рамках тромботической микроангиопатии.
Ключевые слова: нефротоксичность, антиангиогенная терапия, противоопухолевая терапия, нежелательные явления, тромботическая микроангиопатия
Aim. To assess early clinical and laboratory manifestations and risk factors for nephrotoxicity of antiangiogenic drugs.
Materials and methods. The study included 50 patients who received antiangiogenic drugs in different regimens of chemotherapy. Demographic factors, body mass index, blood pressure levels, type of antiangiogenic drug, and concomitant therapy were assessed. Before treatment and over a period of 8 weeks, the levels of hemoglobin, number of platelets and schistocytes, D-dimer levels, serum lactate dehydrogenase (LDH) levels, as well as daily proteinuria and serum creatinine and eGFRCKD-EPI were assessed. Linear regression analysis was performed to assess risk factors for nephrotoxicity and arterial hypertension (AH).
Results. The median age of patients was 46 [34–57] years, 22 (44%) men and 28 (56%) women. AH developed in 52%, a decrease in eGFR – in 42%, along with a decrease in hemoglobin levels and an increase in LDH levels – at 2 weeks of therapy. The numbers of schistocytes and platelets significantly decreased by 8 weeks of therapy. Risk factors for impaired renal function during treatment with antiangiogenic drugs were an initial decrease in GFR less than 80 ml/min/1.73 m2, an increase in D-dimer levels, and a decrease in hemoglobin levels by 8 weeks of treatment. The risk factors for AH during therapy were the initial decrease in eGFR less than 80 ml/min/1.73 m2 and no prophylactic anticoagulant therapy.
Conclusion. Early signs of nephrotoxicity of antiangiogenic anticancer drugs were a decrease in eGFR and AH. The independent risk factors for nephrotoxicity were the initial decrease in eGFR, an increase in D-dimer levels, and a decrease in hemoglobin levels at 8 weeks of treatment, while the prophylactic use of anticoagulant therapy reduced this risk in our study.
Keywords: nephrotoxicity, antiangiogenic therapy, antitumor therapy, adverse events, thrombotic microangiopathy
Цель. Оценить ранние клинико-лабораторные проявления и факторы риска нефротоксичности антиангиогенных противоопухолевых препаратов.
Материалы и методы. В исследование вошли 50 пациентов, получавших антиангиогенные препараты в составе противоопухолевой химиотерапии. Оценивали демографические показатели, индекс массы тела, цифры артериального давления, тип антиангиогенного препарата, сопроводительную терапию. До начала лечения и в динамике в течение 8 нед с помощью критерия Фридмана оценивали уровень гемоглобина, тромбоцитов, шистоцитов, D-димера, лактатдегидрогеназы сыворотки крови, а также суточной протеинурии и креатинина сыворотки крови и расчетной скорости клубочковой фильтрации (СКФ) по CKD-EPI. Для оценки факторов риска нефротоксичности и артериальной гипертензии (АГ) проводили линейный регрессионный анализ.
Результаты. Медиана возраста пациентов составила 46 [34–57] лет, 22 (44%) мужчины и 28 (56%) женщин. АГ развилась у 52%, снижение СКФ – у 42% наряду со снижением гемоглобина и повышением лактатдегидрогеназы на 2-й неделе терапии. Число шистоцитов и тромбоцитов достоверно снизилось к 8-й неделе терапии. Факторами риска нарушения функции почек на фоне лечения антиангиогенными препаратами стали исходное снижение СКФ<80 мл/мин, повышение D-димера, уменьшение гемоглобина к 8-й неделе лечения. Факторами риска формирования АГ на фоне терапии оказались исходное снижение расчетной СКФ<80 мл/мин и отсутствие профилактической антикоагулянтной терапии.
Заключение. Ранними признаками нефротоксичности антиангиогенных противоопухолевых препаратов являлись снижение СКФ и развитие АГ. Независимыми факторами риска нефротоксичности стали исходное снижение СКФ, повышение D-димера и уменьшение гемоглобина на 8-й неделе лечения, в то же время профилактическое применение антикоагулянтной терапии снижало этот риск в нашем исследовании. Данные изменения можно рассматривать в рамках тромботической микроангиопатии.
Ключевые слова: нефротоксичность, антиангиогенная терапия, противоопухолевая терапия, нежелательные явления, тромботическая микроангиопатия
________________________________________________
Aim. To assess early clinical and laboratory manifestations and risk factors for nephrotoxicity of antiangiogenic drugs.
Materials and methods. The study included 50 patients who received antiangiogenic drugs in different regimens of chemotherapy. Demographic factors, body mass index, blood pressure levels, type of antiangiogenic drug, and concomitant therapy were assessed. Before treatment and over a period of 8 weeks, the levels of hemoglobin, number of platelets and schistocytes, D-dimer levels, serum lactate dehydrogenase (LDH) levels, as well as daily proteinuria and serum creatinine and eGFRCKD-EPI were assessed. Linear regression analysis was performed to assess risk factors for nephrotoxicity and arterial hypertension (AH).
Results. The median age of patients was 46 [34–57] years, 22 (44%) men and 28 (56%) women. AH developed in 52%, a decrease in eGFR – in 42%, along with a decrease in hemoglobin levels and an increase in LDH levels – at 2 weeks of therapy. The numbers of schistocytes and platelets significantly decreased by 8 weeks of therapy. Risk factors for impaired renal function during treatment with antiangiogenic drugs were an initial decrease in GFR less than 80 ml/min/1.73 m2, an increase in D-dimer levels, and a decrease in hemoglobin levels by 8 weeks of treatment. The risk factors for AH during therapy were the initial decrease in eGFR less than 80 ml/min/1.73 m2 and no prophylactic anticoagulant therapy.
Conclusion. Early signs of nephrotoxicity of antiangiogenic anticancer drugs were a decrease in eGFR and AH. The independent risk factors for nephrotoxicity were the initial decrease in eGFR, an increase in D-dimer levels, and a decrease in hemoglobin levels at 8 weeks of treatment, while the prophylactic use of anticoagulant therapy reduced this risk in our study.
Keywords: nephrotoxicity, antiangiogenic therapy, antitumor therapy, adverse events, thrombotic microangiopathy
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21. Abrahamson D. Glomerulogenesis in the developing kidney. Semin Nephrol. 1991;4(11):375-89.
22. Eremina V, Baelde H, Quaggin S. Role of the VEGF – a signaling pathway in the glomerulus: evidence for crosstalk between components of the glomerular filtration barrier. Nephron Physiol. 2007;106(2):32-7. DOI:10.1159/000101798
23. Hara A, Wada T, Furuchi K, et al. Blockade of VEGF accelerates proteinuria via decrease in nephrin expression in rat crescentic glomerulonephritis. Kidney Int. 2006;69(11):1986-95. DOI:10.1038/sj.ki.5000439
24. Horowitz J, Rivard A, van der Zee R, et al. Vascular endothelial growth factor/vascular permeability factor produces nitric oxide-dependent hypotension. Evidence for a maintenance role in quiescent adult endothelium. Arterioscler Thromb Vasc Biol. 1997;17:2793-800. DOI:10.1161/01.atv.17.11.2793
25. Bollee G, Patey N, Cazajous G, et al. Thrombotic microangiopathy secondary to VEGF pathway inhibition by sunitinib. Nephrol Dial Transplant. 2009;24:682-5. DOI:10.1093/ndt/gfn657
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29. Hanna R, Barsoum M, Arman F, et al. Nephrotoxicity induced by intravitreal vascular endothelial growth factor inhibitors: emerging evidence. Kidney Int. 2019;96(3):572-80.
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2. Zirlik K, Duyster J. Anti-Angiogenics: Current Situation and Future Perspectives. Oncol Res Treat. 2018;41:166-17. DOI:10.1159/000488087
3. Wang Z, Dabrosin C, Yin X, et al. Broad targeting of angiogenesis for cancer prevention and therapy. Semin Cancer Biol. 2015;35:S224-43. DOI:10.1016/j.semcancer.2015.01.001
4. Balic M, Hilbe W, Gusel S, et al. Prevalence of comorbidity in cancer patients scheduled for systemic anticancer treatment in Austria. Memo. 2019;12:290-6. DOI:10.1007/s12254-019-00542-7
5. Kelly C, Power D, Lichtman S. Targeted Therapy in Older Patients With Solid Tumors. J Clin Oncol. 2014;32(34):2635-42. DOI:10.1200/JCO.2014.55.4246
6. 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;12:391-400. DOI:10.1159/00050071
7.Tryakin AA. Targeted therapy for colorectal cancer, stomach cancer and pancreas. Practical oncology. 2010;11(3):143-50 (in Russian)
8. Giantonio B, Catalano P, Meropol N. 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;20:1539-44. DOI:10.1200/JCO.2006.09.6305
9. 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
10. 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
11. Maitland M, Bakris G, Black H, 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;102:596-604. DOI:10.1093/jnci/djq091
12. Vaidya V, Ozer J, Frank D, 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
13. Arnold D, Fuchs C, Tabernero J, et al. Meta-analysis of individual patient safety data from six randomized, placebo-controlled trials with the antiangiogenic VEGFR2-binding monoclonal antibody ramucirumab. Ann Oncol. 2017;28:2932-42. DOI:10.1093/annonc/mdx514
14. Qi W, Shen Z, Tang L. Risk of Hypertension in Cancer Patients Treated with Aflibercept: A Systematic Review and Meta-Analysis. Clin Drug Investig. 2014;34:231-40. DOI:10.1007/s40261-014-0174-5
15. Azad N, Posadas E, Kwitkowski V, et al. Combination targeted therapy with sorafenib and bevacizumab results in enhanced toxicity and antitumor activity. J Clin Oncol. 2008;26:3709-14. DOI:10.1200/JCO.2007.10.8332
16. Feldman D, Baum M, Ginsberg M, et al. Phase I trial of bevacizumab plus escalated doses ofsunitinib in patients with metastatic renal cell carcinoma. J Clin Oncol. 2009;27:1432-9. DOI:10.1200/JCO.2008.19.0108
17. Wu S, Chen J, Kudelka A, et al. Incidence and risk of hypertension with sorafenib in patients with cancer: a systematic review and meta-analysis. Lancet Oncol. 2008;9:117-23. DOI:10.1016/j.eururo.2018.05.002
18. Kanbayashi Y, Ishikawa T, Tabuchi Y, et al. Predictive factors for the development of proteinuria in cancer patients treated with bevacizumab, ramucirumab, and aflibercept: a single-institution retrospective analysis. Sci Rep. 2020;10:2011. DOI:10.1038/s41598-020-58994-5
19. Slusarz K, Merker V, Muzikansky A, et al. Long-term toxicity of bevacizumab therapy in neurofibromatosis 2 patients. Cancer Chemother Pharmacol. 2014;73(6):1197-204. DOI:10.1007/s00280-014-2456-2
20. Vaidya V, Ozer J, Frank D, 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
21. Abrahamson D. Glomerulogenesis in the developing kidney. Semin Nephrol. 1991;4(11):375-89.
22. Eremina V, Baelde H, Quaggin S. Role of the VEGF – a signaling pathway in the glomerulus: evidence for crosstalk between components of the glomerular filtration barrier. Nephron Physiol. 2007;106(2):32-7. DOI:10.1159/000101798
23. Hara A, Wada T, Furuchi K, et al. Blockade of VEGF accelerates proteinuria via decrease in nephrin expression in rat crescentic glomerulonephritis. Kidney Int. 2006;69(11):1986-95. DOI:10.1038/sj.ki.5000439
24. Horowitz J, Rivard A, van der Zee R, et al. Vascular endothelial growth factor/vascular permeability factor produces nitric oxide-dependent hypotension. Evidence for a maintenance role in quiescent adult endothelium. Arterioscler Thromb Vasc Biol. 1997;17:2793-800. DOI:10.1161/01.atv.17.11.2793
25. Bollee G, Patey N, Cazajous G, et al. Thrombotic microangiopathy secondary to VEGF pathway inhibition by sunitinib. Nephrol Dial Transplant. 2009;24:682-5. DOI:10.1093/ndt/gfn657
26. Izzedine H, Brocheriou I, Deray G, Rixe O. Thrombotic microangiopathy and anti-VEGF agents. Nephrol Dial Transplant. 2007;22:1481-2. DOI:10.1093/ndt.gfl565
27. Estrada C, Maldonado A, Mallipattu S. Therapeutic Inhibition of VEGF Signaling and Associated Nephrotoxicities. JASN. 2019;30(2):187-200. DOI:10.1681/ASN.2018080853
28. Fujii T, Kawaasoe K, Tonooka A, et al. Nephrotic syndrome associated with ramucirumab therapy. A single-center case series and literature review. Medicine (Baltimore). 2019;98(27):e16236. DOI:10.1097/MD.0000000000016236
29. Hanna R, Barsoum M, Arman F, et al. Nephrotoxicity induced by intravitreal vascular endothelial growth factor inhibitors: emerging evidence. Kidney Int. 2019;96(3):572-80.
DOI:10.1016/j.kint.2019.02.042
30. Diabetic Retinopathy Clinical Research Network, Scott IU, Edwards AR, et al. A phase II randomized clinical trial of intravitreal bevacizumab for diabetic macular edema. Ophthalmology. 2007;114(10):1860-7. DOI:10.1016/j.ophtha.2007.05.062
31. Georgalas I, Papaconstantinou D, Papadopoulos K, et al. Renal Injury Following Intravitreal Anti-VEGF Administration in Diabetic Patients with Proliferative Diabetic Retinopathy and Chronic Kidney Disease – A Possible Side Effect? Curr Drug Saf. 2014;9:156. DOI:10.2174/1574886309666140211113635
32. Khneizer P, Gebran T, Al-Taee M, et al. Self-limited membranous nephropathy after intravitreal bevacizumab therapy for age-related macular degeneration. J Nephropathol. 2017;6(3):134-7.DOI:10.15171/jnp.2017.23
33. Morale E, Moliz C, Gutierrez E. Renal damage associated to intravitreal administration of ranibizumab. Nefrología (English Edition). 2017;37(6):653-5. DOI:10.1016/j.nefroe.2017.10.007
34. Wang J, Zhu C. Anticoagulation in combination with antiangiogenesis and chemotherapy for cancer patients: evidence and hypothesis. Onco Targets Ther. 2016;9:4737-46. DOI:10.2147/OTT.S103184
35. Frere C, Debourdeau P, Hij A, et al. Therapy for cancer-related thromboembolism. Semin Oncol. 2014;41(3):319-38. DOI:10.1053/j.seminoncol.2014.04.005
36. Kilickap S, Abali H, Celik I. Bevacizumab, bleeding, thrombosis, and warfarin. J Clin Oncol. 2003;21(18):3542. DOI:10.1200/JCO.2003.99.046
2. Zirlik K, Duyster J. Anti-Angiogenics: Current Situation and Future Perspectives. Oncol Res Treat. 2018;41:166-17. DOI:10.1159/000488087
3. Wang Z, Dabrosin C, Yin X, et al. Broad targeting of angiogenesis for cancer prevention and therapy. Semin Cancer Biol. 2015;35:S224-43. DOI:10.1016/j.semcancer.2015.01.001
4. Balic M, Hilbe W, Gusel S, et al. Prevalence of comorbidity in cancer patients scheduled for systemic anticancer treatment in Austria. Memo. 2019;12:290-6. DOI:10.1007/s12254-019-00542-7
5. Kelly C, Power D, Lichtman S. Targeted Therapy in Older Patients With Solid Tumors. J Clin Oncol. 2014;32(34):2635-42. DOI:10.1200/JCO.2014.55.4246
6. 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;12:391-400. DOI:10.1159/00050071
7. Трякин А.А. Таргетная терапия колоректального рака, рака желудка и поджелудочной железы. Практ. онкология. 2010;11(3):143-50 [Tryakin AA. Targeted therapy for colorectal cancer, stomach cancer and pancreas. Practical oncology. 2010;11(3):143-50 (in Russian)].
8. Giantonio B, Catalano P, Meropol N. 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;20:1539-44. DOI:10.1200/JCO.2006.09.6305
9. 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
10. 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
11. Maitland M, Bakris G, Black H, 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;102:596-604. DOI:10.1093/jnci/djq091
12. Vaidya V, Ozer J, Frank D, 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
13. Arnold D, Fuchs C, Tabernero J, et al. Meta-analysis of individual patient safety data from six randomized, placebo-controlled trials with the antiangiogenic VEGFR2-binding monoclonal antibody ramucirumab. Ann Oncol. 2017;28:2932-42. DOI:10.1093/annonc/mdx514
14. Qi W, Shen Z, Tang L. Risk of Hypertension in Cancer Patients Treated with Aflibercept: A Systematic Review and Meta-Analysis. Clin Drug Investig. 2014;34:231-40. DOI:10.1007/s40261-014-0174-5
15. Azad N, Posadas E, Kwitkowski V, et al. Combination targeted therapy with sorafenib and bevacizumab results in enhanced toxicity and antitumor activity. J Clin Oncol. 2008;26:3709-14. DOI:10.1200/JCO.2007.10.8332
16. Feldman D, Baum M, Ginsberg M, et al. Phase I trial of bevacizumab plus escalated doses ofsunitinib in patients with metastatic renal cell carcinoma. J Clin Oncol. 2009;27:1432-9. DOI:10.1200/JCO.2008.19.0108
17. Wu S, Chen J, Kudelka A, et al. Incidence and risk of hypertension with sorafenib in patients with cancer: a systematic review and meta-analysis. Lancet Oncol. 2008;9:117-23. DOI:10.1016/j.eururo.2018.05.002
18. Kanbayashi Y, Ishikawa T, Tabuchi Y, et al. Predictive factors for the development of proteinuria in cancer patients treated with bevacizumab, ramucirumab, and aflibercept: a single-institution retrospective analysis. Sci Rep. 2020;10:2011. DOI:10.1038/s41598-020-58994-5
19. Slusarz K, Merker V, Muzikansky A, et al. Long-term toxicity of bevacizumab therapy in neurofibromatosis 2 patients. Cancer Chemother Pharmacol. 2014;73(6):1197-204. DOI:10.1007/s00280-014-2456-2
20. Vaidya V, Ozer J, Frank D, 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
21. Abrahamson D. Glomerulogenesis in the developing kidney. Semin Nephrol. 1991;4(11):375-89.
22. Eremina V, Baelde H, Quaggin S. Role of the VEGF – a signaling pathway in the glomerulus: evidence for crosstalk between components of the glomerular filtration barrier. Nephron Physiol. 2007;106(2):32-7. DOI:10.1159/000101798
23. Hara A, Wada T, Furuchi K, et al. Blockade of VEGF accelerates proteinuria via decrease in nephrin expression in rat crescentic glomerulonephritis. Kidney Int. 2006;69(11):1986-95. DOI:10.1038/sj.ki.5000439
24. Horowitz J, Rivard A, van der Zee R, et al. Vascular endothelial growth factor/vascular permeability factor produces nitric oxide-dependent hypotension. Evidence for a maintenance role in quiescent adult endothelium. Arterioscler Thromb Vasc Biol. 1997;17:2793-800. DOI:10.1161/01.atv.17.11.2793
25. Bollee G, Patey N, Cazajous G, et al. Thrombotic microangiopathy secondary to VEGF pathway inhibition by sunitinib. Nephrol Dial Transplant. 2009;24:682-5. DOI:10.1093/ndt/gfn657
26. Izzedine H, Brocheriou I, Deray G, Rixe O. Thrombotic microangiopathy and anti-VEGF agents. Nephrol Dial Transplant. 2007;22:1481-2. DOI:10.1093/ndt.gfl565
27. Estrada C, Maldonado A, Mallipattu S. Therapeutic Inhibition of VEGF Signaling and Associated Nephrotoxicities. JASN. 2019;30(2):187-200. DOI:10.1681/ASN.2018080853
28. Fujii T, Kawaasoe K, Tonooka A, et al. Nephrotic syndrome associated with ramucirumab therapy. A single-center case series and literature review. Medicine (Baltimore). 2019;98(27):e16236. DOI:10.1097/MD.0000000000016236
29. Hanna R, Barsoum M, Arman F, et al. Nephrotoxicity induced by intravitreal vascular endothelial growth factor inhibitors: emerging evidence. Kidney Int. 2019;96(3):572-80.
DOI:10.1016/j.kint.2019.02.042
30. Diabetic Retinopathy Clinical Research Network, Scott IU, Edwards AR, et al. A phase II randomized clinical trial of intravitreal bevacizumab for diabetic macular edema. Ophthalmology. 2007;114(10):1860-7. DOI:10.1016/j.ophtha.2007.05.062
31. Georgalas I, Papaconstantinou D, Papadopoulos K, et al. Renal Injury Following Intravitreal Anti-VEGF Administration in Diabetic Patients with Proliferative Diabetic Retinopathy and Chronic Kidney Disease – A Possible Side Effect? Curr Drug Saf. 2014;9:156. DOI:10.2174/1574886309666140211113635
32. Khneizer P, Gebran T, Al-Taee M, et al. Self-limited membranous nephropathy after intravitreal bevacizumab therapy for age-related macular degeneration. J Nephropathol. 2017;6(3):134-7.DOI:10.15171/jnp.2017.23
33. Morale E, Moliz C, Gutierrez E. Renal damage associated to intravitreal administration of ranibizumab. Nefrología (English Edition). 2017;37(6):653-5. DOI:10.1016/j.nefroe.2017.10.007
34. Wang J, Zhu C. Anticoagulation in combination with antiangiogenesis and chemotherapy for cancer patients: evidence and hypothesis. Onco Targets Ther. 2016;9:4737-46. DOI:10.2147/OTT.S103184
35. Frere C, Debourdeau P, Hij A, et al. Therapy for cancer-related thromboembolism. Semin Oncol. 2014;41(3):319-38. DOI:10.1053/j.seminoncol.2014.04.005
36. Kilickap S, Abali H, Celik I. Bevacizumab, bleeding, thrombosis, and warfarin. J Clin Oncol. 2003;21(18):3542. DOI:10.1200/JCO.2003.99.046
________________________________________________
2. Zirlik K, Duyster J. Anti-Angiogenics: Current Situation and Future Perspectives. Oncol Res Treat. 2018;41:166-17. DOI:10.1159/000488087
3. Wang Z, Dabrosin C, Yin X, et al. Broad targeting of angiogenesis for cancer prevention and therapy. Semin Cancer Biol. 2015;35:S224-43. DOI:10.1016/j.semcancer.2015.01.001
4. Balic M, Hilbe W, Gusel S, et al. Prevalence of comorbidity in cancer patients scheduled for systemic anticancer treatment in Austria. Memo. 2019;12:290-6. DOI:10.1007/s12254-019-00542-7
5. Kelly C, Power D, Lichtman S. Targeted Therapy in Older Patients With Solid Tumors. J Clin Oncol. 2014;32(34):2635-42. DOI:10.1200/JCO.2014.55.4246
6. 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;12:391-400. DOI:10.1159/00050071
7.Tryakin AA. Targeted therapy for colorectal cancer, stomach cancer and pancreas. Practical oncology. 2010;11(3):143-50 (in Russian)
8. Giantonio B, Catalano P, Meropol N. 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;20:1539-44. DOI:10.1200/JCO.2006.09.6305
9. 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
10. 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
11. Maitland M, Bakris G, Black H, 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;102:596-604. DOI:10.1093/jnci/djq091
12. Vaidya V, Ozer J, Frank D, 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
13. Arnold D, Fuchs C, Tabernero J, et al. Meta-analysis of individual patient safety data from six randomized, placebo-controlled trials with the antiangiogenic VEGFR2-binding monoclonal antibody ramucirumab. Ann Oncol. 2017;28:2932-42. DOI:10.1093/annonc/mdx514
14. Qi W, Shen Z, Tang L. Risk of Hypertension in Cancer Patients Treated with Aflibercept: A Systematic Review and Meta-Analysis. Clin Drug Investig. 2014;34:231-40. DOI:10.1007/s40261-014-0174-5
15. Azad N, Posadas E, Kwitkowski V, et al. Combination targeted therapy with sorafenib and bevacizumab results in enhanced toxicity and antitumor activity. J Clin Oncol. 2008;26:3709-14. DOI:10.1200/JCO.2007.10.8332
16. Feldman D, Baum M, Ginsberg M, et al. Phase I trial of bevacizumab plus escalated doses ofsunitinib in patients with metastatic renal cell carcinoma. J Clin Oncol. 2009;27:1432-9. DOI:10.1200/JCO.2008.19.0108
17. Wu S, Chen J, Kudelka A, et al. Incidence and risk of hypertension with sorafenib in patients with cancer: a systematic review and meta-analysis. Lancet Oncol. 2008;9:117-23. DOI:10.1016/j.eururo.2018.05.002
18. Kanbayashi Y, Ishikawa T, Tabuchi Y, et al. Predictive factors for the development of proteinuria in cancer patients treated with bevacizumab, ramucirumab, and aflibercept: a single-institution retrospective analysis. Sci Rep. 2020;10:2011. DOI:10.1038/s41598-020-58994-5
19. Slusarz K, Merker V, Muzikansky A, et al. Long-term toxicity of bevacizumab therapy in neurofibromatosis 2 patients. Cancer Chemother Pharmacol. 2014;73(6):1197-204. DOI:10.1007/s00280-014-2456-2
20. Vaidya V, Ozer J, Frank D, 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
21. Abrahamson D. Glomerulogenesis in the developing kidney. Semin Nephrol. 1991;4(11):375-89.
22. Eremina V, Baelde H, Quaggin S. Role of the VEGF – a signaling pathway in the glomerulus: evidence for crosstalk between components of the glomerular filtration barrier. Nephron Physiol. 2007;106(2):32-7. DOI:10.1159/000101798
23. Hara A, Wada T, Furuchi K, et al. Blockade of VEGF accelerates proteinuria via decrease in nephrin expression in rat crescentic glomerulonephritis. Kidney Int. 2006;69(11):1986-95. DOI:10.1038/sj.ki.5000439
24. Horowitz J, Rivard A, van der Zee R, et al. Vascular endothelial growth factor/vascular permeability factor produces nitric oxide-dependent hypotension. Evidence for a maintenance role in quiescent adult endothelium. Arterioscler Thromb Vasc Biol. 1997;17:2793-800. DOI:10.1161/01.atv.17.11.2793
25. Bollee G, Patey N, Cazajous G, et al. Thrombotic microangiopathy secondary to VEGF pathway inhibition by sunitinib. Nephrol Dial Transplant. 2009;24:682-5. DOI:10.1093/ndt/gfn657
26. Izzedine H, Brocheriou I, Deray G, Rixe O. Thrombotic microangiopathy and anti-VEGF agents. Nephrol Dial Transplant. 2007;22:1481-2. DOI:10.1093/ndt.gfl565
27. Estrada C, Maldonado A, Mallipattu S. Therapeutic Inhibition of VEGF Signaling and Associated Nephrotoxicities. JASN. 2019;30(2):187-200. DOI:10.1681/ASN.2018080853
28. Fujii T, Kawaasoe K, Tonooka A, et al. Nephrotic syndrome associated with ramucirumab therapy. A single-center case series and literature review. Medicine (Baltimore). 2019;98(27):e16236. DOI:10.1097/MD.0000000000016236
29. Hanna R, Barsoum M, Arman F, et al. Nephrotoxicity induced by intravitreal vascular endothelial growth factor inhibitors: emerging evidence. Kidney Int. 2019;96(3):572-80.
DOI:10.1016/j.kint.2019.02.042
30. Diabetic Retinopathy Clinical Research Network, Scott IU, Edwards AR, et al. A phase II randomized clinical trial of intravitreal bevacizumab for diabetic macular edema. Ophthalmology. 2007;114(10):1860-7. DOI:10.1016/j.ophtha.2007.05.062
31. Georgalas I, Papaconstantinou D, Papadopoulos K, et al. Renal Injury Following Intravitreal Anti-VEGF Administration in Diabetic Patients with Proliferative Diabetic Retinopathy and Chronic Kidney Disease – A Possible Side Effect? Curr Drug Saf. 2014;9:156. DOI:10.2174/1574886309666140211113635
32. Khneizer P, Gebran T, Al-Taee M, et al. Self-limited membranous nephropathy after intravitreal bevacizumab therapy for age-related macular degeneration. J Nephropathol. 2017;6(3):134-7.DOI:10.15171/jnp.2017.23
33. Morale E, Moliz C, Gutierrez E. Renal damage associated to intravitreal administration of ranibizumab. Nefrología (English Edition). 2017;37(6):653-5. DOI:10.1016/j.nefroe.2017.10.007
34. Wang J, Zhu C. Anticoagulation in combination with antiangiogenesis and chemotherapy for cancer patients: evidence and hypothesis. Onco Targets Ther. 2016;9:4737-46. DOI:10.2147/OTT.S103184
35. Frere C, Debourdeau P, Hij A, et al. Therapy for cancer-related thromboembolism. Semin Oncol. 2014;41(3):319-38. DOI:10.1053/j.seminoncol.2014.04.005
36. Kilickap S, Abali H, Celik I. Bevacizumab, bleeding, thrombosis, and warfarin. J Clin Oncol. 2003;21(18):3542. DOI:10.1200/JCO.2003.99.046
Авторы
К.С. Гречухина*1,2, Н.В. Чеботарева3, Л.Г. Жукова2, Т.Н. Краснова1
1ФГБОУ ВО «Московский государственный университет им. М.В. Ломоносова», Москва, Россия;
2ГБУЗ «Московский клинический научно-практический центр им. А.С. Логинова» Департамента здравоохранения г. Москвы, Москва, Россия;
3ФГАОУ 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 and Practical Center, Moscow, Russia;
3 Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia
*dr.grechukhina@gmail.com
1ФГБОУ ВО «Московский государственный университет им. М.В. Ломоносова», Москва, Россия;
2ГБУЗ «Московский клинический научно-практический центр им. А.С. Логинова» Департамента здравоохранения г. Москвы, Москва, Россия;
3ФГАОУ 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 and Practical Center, Moscow, Russia;
3 Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia
*dr.grechukhina@gmail.com
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