Современные тенденции в диагностике и лечении иммуновоспалительных заболеваний почек: трансляция фундаментальных открытий в клиническую практику - Журнал Терапевтический архив №12 Vario 2023

Современные тенденции в диагностике и лечении иммуновоспалительных заболеваний почек: трансляция фундаментальных открытий в клиническую практику

Буланов Н.М., Моисеев С.В. Современные тенденции в диагностике и лечении иммуновоспалительных заболеваний почек: трансляция фундаментальных открытий в клиническую практику. Терапевтический архив. 2023;95(12):1075–1082. DOI: 10.26442/00403660.2023.12.202502

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Bulanov NM, Moiseev SV. State-of-the-art trends in the treatment of immune-mediated inflammatory kidney diseases: Translation of the fundamental science into clinical practice. A review. Terapevticheskii Arkhiv (Ter. Arkh.). 2023;95(12):1075–1082. DOI: 10.26442/00403660.2023.12.202502

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Аннотация

Гломеруло- и тубулоинтерстициальные нефриты – не ведущая причина развития хронической болезни почек в популяции, но сложности их диагностики и лечения, а также более быстрые по сравнению с сахарным диабетом и артериальной гипертензией темпы прогрессирования почечной дисфункции обосновывают актуальность решения этой проблемы для внутренней медицины. Благодаря фундаментальным открытиям в области морфологии и патофизиологии, а также внедрению различных методов лабораторного и инструментального обследования во второй половине XX в. стал возможным существенный прогресс в диагностике и лечении этой группы заболеваний. Современные стандарты диагностики подразумевают комплексную оценку клинико-лабораторных и гистологических данных с целью верификации нозологической формы заболевания. Накопление знаний о патогенезе этой группы нозологий привело к очередному пересмотру подхода к классификации гломерулонефритов, в основе которого должен лежать патогенетический принцип с выделением фенотипов, ассоциированных с инфекциями, аутоиммунными, аутовоспалительными и аллоиммунными реакциями, а также моноклональной гаммапатией, с обязательной оценкой активности иммунного воспаления и склеротических изменений (хронизация) в ткани почки. Стал возможным персонализированный выбор оптимальной тактики лечения на основании не только нозологической формы, но и тяжести течения заболевания, а также индивидуальных особенностей пациента. При этом ведущими тенденциями становятся рациональное применение глюкокортикостероидов (стероид-сберегающие схемы) и неселективных цитостатиков, в первую очередь циклофосфамида, а также внедрение мультитаргетных схем лечения, в том числе с использованием биологических препаратов и малых молекул, избирательно подавляющих B-лимфоциты или различные пути активации системы комплемента. Помимо иммуносупрессивной терапии обязательным компонентом лечения стала нефропротективная терапия, основанная на применении не только традиционных антагонистов ренин-ангиотензин-альдостероновой системы, но и антагонистов эндотелиновых рецепторов, а также ингибиторов натрийглюкозного котранспортера 2-го типа. Не меньшее значение придается немедикаментозным компонентам нефропротективной стратегии. Рациональная комбинация этих подходов позволяет оптимизировать подходы к ведению пациентов с иммуновоспалительными заболеваниями почек, однако требует от врача глубокой подготовки и приверженности зафиксированным в рекомендациях принципам.

Ключевые слова: гломерулонефрит, тубулоинтерстициальный нефрит, иммуносупрессивная терапия, нефропротективная терапия, хроническая болезнь почек

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Immune-mediated kidney diseases like glomerulonephritis and tubulointerstitial nephritis are not the most common cause of chronic kidney disease in the population, however the difficulties in their management, as well as a more rapid deterioration of kidney function, compared to diabetes mellitus and hypertension, justify the importance of this problem for internal medicine. Due to the fundamental discoveries in pathology and to the introduction of various methods of laboratory and instrumental investigation in the second half of the XX century substantial progress was made in the diagnostic approaches and treatment of these conditions. State-of-the-art diagnostic approach requires complex evaluation of the clinical, laboratory and morphological data to identify the nosological form of the disease. The accumulation of knowledge in the field of diseases’ pathogenesis led to the revision of the current classification of glomerulonephritis that should be based on the immunopathogenesis of these conditions. The following phenotypes were suggested: autoimmunity-related, autoinflammation-related, alloimmunity-related, infections-related, and monoclonal gammopathy-related. The assessment of disease activity and chronicity in the kidney tissue should be mandatory. Personalized selection of the optimal treatment modality on the basis of the diagnosis, severity, and individual features of the patient is currently possible. The leading trends include rational prescription of glucocorticoids (steroid-sparing regimens) and cytotoxic agents, e.g. cyclophosphamide, as well as the introduction of multitarget regimens that include biologic agents or small molecules selectively suppressing B-cells or various complement pathways. Another mandatory component of treatment on par with immune suppression is nephroprotective therapy, which currently comprises not only traditional renin-angiotensin-aldosterone antagonists, but also endothelin receptor antagonists and sodium-glucose cotransporter-2 inhibitors. Current guidelines emphasize the importance of the non-pharmacological interventions for the implementation of the nephroprotective strategy. Rational combination of the aforementioned approaches allows for the optimization of the management of patients with immune-mediated kidney diseases, although it requires high competencies and strict adherence to the principles of the evidence-based medicine from the healthcare providers.

Keywords: glomerulonephritis, tubulointerstitial nephritis, immune suppressive therapy, nephroprotection, chronic kidney disease

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69. Uhlin F, Szpirt W, Kronbichler A, et al. Endopeptidase cleavage of anti-glomerular basement membrane antibodies in vivo in severe kidney disease: An open-label phase 2a study. J Am Soc Nephrol. 2022;33(4):829-38. DOI:10.1681/ASN.2021111460
70. Li ZH, Guo XY, Quan XY, et al. The role of parietal epithelial cells in the pathogenesis of podocytopathy. Front Physiol. 2022;13:832772. DOI:10.3389/FPHYS.2022.832772
71. Melica ME, Antonelli G, Semeraro R, et al. Differentiation of crescent-forming kidney progenitor cells into podocytes attenuates severe glomerulonephritis in mice. Sci Transl Med. 2022;14(657). DOI:10.1126/SCITRANSLMED.ABG3277
72. Ruggenenti P, Perna A, Mosconi L, et al. Randomised placebo-controlled trial of effect of ramipril on decline in glomerular filtration rate and risk of terminal renal failure in proteinuric, non-diabetic nephropathy. The GISEN Group (Gruppo Italiano di Studi Epidemiologici in Nefrologia). Lancet. 1997;349(9069):1857-63. DOI:10.1016/S0140-6736(96)11445-8
73. Taguma Y, Kitamoto Y, Futaki G, et al. Effect of captopril on heavy proteinuria in azotemic diabetics. N Engl J Med. 1985;313(26):1617-20. DOI:10.1056/NEJM198512263132601
74. Pitcher D, Braddon F, Hendry B, et al. Long-term outcomes in IgA nephropathy. Clin J Am Soc Nephrol. 2023;18(6):727-38. DOI:10.2215/CJN.0000000000000135
75. Caravaca-Fontán F, Stevens K, Padrón M, et al. Sodium-glucose cotransporter 2 inhibition in primary and secondary glomerulonephritis. Nephrol Dial Transplant. 2023:gfad175. DOI:10.1093/ndt/gfad175
76. Heerspink HJL, Radhakrishnan J, Alpers CE, et al. Sparsentan in patients with IgA nephropathy: A prespecified interim analysis from a randomised, double-blind, active-controlled clinical trial. Lancet. 2023;401(10388):1584-94. DOI:10.1016/S0140-6736(23)00569-X
77. Stern EP, Host LV, Wanjiku I, et al. Zibotentan in systemic sclerosis-associated chronic kidney disease: A phase II randomised placebo-controlled trial. Arthritis Res Ther. 2022;24(1):130. DOI:10.1186/S13075-022-02818-6

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72. Ruggenenti P, Perna A, Mosconi L, et al. Randomised placebo-controlled trial of effect of ramipril on decline in glomerular filtration rate and risk of terminal renal failure in proteinuric, non-diabetic nephropathy. The GISEN Group (Gruppo Italiano di Studi Epidemiologici in Nefrologia). Lancet. 1997;349(9069):1857-63. DOI:10.1016/S0140-6736(96)11445-8
73. Taguma Y, Kitamoto Y, Futaki G, et al. Effect of captopril on heavy proteinuria in azotemic diabetics. N Engl J Med. 1985;313(26):1617-20. DOI:10.1056/NEJM198512263132601
74. Pitcher D, Braddon F, Hendry B, et al. Long-term outcomes in IgA nephropathy. Clin J Am Soc Nephrol. 2023;18(6):727-38. DOI:10.2215/CJN.0000000000000135
75. Caravaca-Fontán F, Stevens K, Padrón M, et al. Sodium-glucose cotransporter 2 inhibition in primary and secondary glomerulonephritis. Nephrol Dial Transplant. 2023:gfad175. DOI:10.1093/ndt/gfad175
76. Heerspink HJL, Radhakrishnan J, Alpers CE, et al. Sparsentan in patients with IgA nephropathy: A prespecified interim analysis from a randomised, double-blind, active-controlled clinical trial. Lancet. 2023;401(10388):1584-94. DOI:10.1016/S0140-6736(23)00569-X
77. Stern EP, Host LV, Wanjiku I, et al. Zibotentan in systemic sclerosis-associated chronic kidney disease: A phase II randomised placebo-controlled trial. Arthritis Res Ther. 2022;24(1):130. DOI:10.1186/S13075-022-02818-6

Авторы

Н.М. Буланов*, С.В. Моисеев

ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет), Москва, Россия
*bulanov_n_m@staff.sechenov.ru

________________________________________________

Nikolay M. Bulanov*, Sergey V. Moiseev

Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia
*bulanov_n_m@staff.sechenov.ru

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