Мембранопролиферативный гломерулонефрит в российской популяции
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Материалы и методы. В период 2000–2017 гг. ретроспективно выявляли случаи МПГН с анализом этиологии, клинических данных и морфологии (включая депозиты иммуноглобулинов – Ig – и С3-фракции комплемента). В исследование включено 214 случаев МПГН. Средний возраст пациентов – 44±16 лет. Оценивали достижение полных и частичных ремиссий (ПР, ЧР), общую выживаемость, прогрессирование (по композитной конечной точке: снижение расчетной скорости клубочковой фильтрации – рСКФ – на 50% и более от исходной, или рСКФ <15 мл/мин/1,73 м2, или начало диализа).
Результаты и обсуждение. Нефротический синдром выявлен у 72% больных; в 58,4% случаев рСКФ достигала <60 мл/мин/1,73 м2. Распространенность случаев МПГН среди морфологически подтвержденных гломерулопатий составила 9,3%. Идиопатический МПГН (иМПГН) выявлен в 30,4% случаев, вторичный МПГН (вМПГН) – в 69,6% (аутоиммунные заболевания – 34,1%, инфекционные – 16,4%, моноклональные гаммапатии – 9,3%, комплемент-опосредованные повреждения – 9,8%). Ig+C3+МПГН чаще выявляли на фоне аутоиммунных заболеваний и инфекций. В большинстве случаев Ig-C3+МПГН установлен диагноз С3-гломерулопатии или тромботической микроангиопатии. Этиология Ig-C3-/Ig+C3-МПГН гетерогенна. Медиана периода наблюдения составила 28 [7; 37] мес. Десятилетная общая кумулятивная выживаемость и «почечная» выживаемость составили 71 и 50% соответственно (без различий между иМПГН и вМПГН). В общей группе МПГН частота ПР/ЧР составила 50% (иМПГН – 46,2%, вМПГН – 51,3%) и различалась в зависимости от этиологии МПГН (Рanova=0,049). Кумулятивная выживаемость без прогрессирования в общей группе МПГН в течение 10-летнего периода близка к 100% в случаях достижения ПР/ЧР и 0% – при отсутствии ремиссии.
Заключение. Синдром МПГН представляет собой тяжелый вариант повреждения клубочков с гетерогенной этиологической структурой и серьезным прогнозом. Целенаправленная клинико-морфологическая диагностика позволяет идентифицировать причину МПГН в большинстве случаев, что является основой для выбора адекватного лечения и улучшения исходов.
Ключевые слова: мембранопролиферативный гломерулонефрит, этиология, морфология, клиническая картина, лечение, прогрессирование, полная ремиссия, частичная ремиссия.
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Aim. Analysis of etiology, clinical and morphological manifestations, approaches to therapy and prognosis of membranoproliferative glomerulonephritis (MPGN).
Materials and methods. Cases of MPGN were retrospectively identified in the period 2000–2017 with subsequent analysis of etiology, clinical data and morphology (including deposits of immunoglobulins (Ig) and C3 complement fractions). The achievement of complete and partial remissions (PR, CR), overall survival, progression (by composite endpoint: decrease in the estimated GFR (eGFR) ≥50% from the baseline or eGFR <15 ml/min/1.73 m2 or the onset of dialysis).
Results and discussion. 214 cases of MPGN entered the study with the average age of 44±16 years. Most patients had nephrotic syndrome and significant hematuria. In 58.4% of cases, eGFR was <60 mL/min/1.73 m2, and every fifth patient had CKD 4 or 5 stages. The prevalence of MPGN among all biopsy-confirmed glomerulopathies was 9.3%. Idiopathic MPGN (iMPGN) was detected in 30.4% of cases, secondary MSGN (sMPGN) – in 69.6% (autoimmune diseases – 34.1%, infectious diseases – 16.4%, monoclonal gammopathies – 9.3%, complement-mediated damage – 9.8%). Ig+C3+MPGN was mainly associated with autoimmune diseases and infections; C3-glomerulopathy or thrombotic microangiopathy were most often causes of Ig-C3+MPGN; Ig-C3-/Ig+C3-MPGN had heterogeneous etiology. The median follow-up period was 28 [7; 37] months. The 10-year total cumulative patient and renal survival rates were 71 and 50%, respectively (without differences between sMPGN and iMPGN). The frequency of the PR/CR was 50% (iMPGN – 46.2%, sMPGN – 51.3%) depending on the etiology of the MPGN (p=0.049). The cumulative 10-year progression-free renal survival was nearly 100% in cases with PR/CR and 0% in non-responders.
Conclusion. MPGN is a severe variant of glomerular damage with a heterogeneous etiological structure and an unfavorable prognosis. Targeted clinical and morphological diagnostics of MPGN allows to identify the cause of the disease in most cases. This approach is reliable for the adequate treatment choice and improvement of outcomes in MPGN.
Keywords: membranoproliferative glomerulonephritis, etiology, morphology, immunomorphology, clinical manifestations, complete remissions, partial remissions, therapy, prognosis, survival.
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23. Hou J, Markowitz GS, Bomback AS, Appel GB, Herlitz LC, Barry Stokes M, d'Agati VD. Toward a working definition of C3 glomerulopathy by immunofluorescence. Kidney Int. 2014;85(2):450-6. doi: 10.1038/ki.2013.340
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25. Palmer SC, Tunnicliffe DJ, Singh-Grewal D, Mavridis D, Tonelli M, Johnson DW, et al. Induction and Maintenance Immunosuppression Treatment of Proliferative Lupus Nephritis: A Network Meta-analysis of Randomized Trials. Am J Kidney Dis. 2017;70(3):324-36. doi: 10.1053/j.ajkd.2016.12.008
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1. Sethi S, Fervenza FC. Membranoproliferative glomerulonephritis: Pathogenetic heterogeneity and proposal for a new classification. Semin Nephrol. 2011;31:341-8. doi: 10.1016/j.semnephrol.2011.06.005
2. Cook HT, Pickering MC. Histopathology of MPGN and C3 glomerulopathies. Nat Rev Nephrol. 2015;11(1):14-22. doi: 10.1038/nrneph.2014.217
3. Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis Work Group: KDIGO Clinical Practice Guideline for Glomerulonephritis. Kidney Int Suppl. 2012;2:139-274. doi: 10.1038/kisup.2012.1
4. [Smirnov AV, Dobronravov VA, Sipovskii VG, Trofimenko II, Pirozhkov IA, Kayukov IG, Lebedev KI. Clinical practice guideline for diagnostics, treatment and prognosis of membranoproliferative glomerulonephritis. Nefrologiya. 2014;18(6):82-93 (In Russ.)]. http://journal.nephrolog.ru/jour/article/view/63
5. Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF, Feldman HI, et al. CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration). A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150(9):604-12. doi: 10.7326/0003-4819-150-9-200905050-00006
6. Nargund P, Kambham N, Mehta K, Lafayette RA. Clinicopathological features of membranoproliferative glomerulonephritis under a new classification. Clin Nephrol. 2015;84(6):323-30. doi: 10.5414/cn108619
7. Pavinic J, Miglinas M. The incidence of possible causes of membranoproliferative glomerulonephritis: a single-center experience. Hippokratia. 2015;19(4):314-8.
8. Nakagawa N, Hasebe N, Hattori M, Nagata M, Yokoyama H, Sato H, et al. Clinical features and pathogenesis of membranoproliferative glomerulonephritis: a nationwide analysis of the Japan renal biopsy registry from 2007 to 2015. Clin Exp Nephrol. 2017. doi: 10.1007/s10157-017-1513-7
9. Anders HJ, Fogo AB. Immunopathology of lupus nephritis. Semin Immunopathol. 2014;36(4):443-59. doi: 10.1007/s00281-013-0413-5
10. Haas M. Histologic subclassification of IgA nephropathy: A clinicopathologic study of 244 cases. Am J Kidney Dis. 1997;29:829-42. doi: 10.1016/s0272-6386(97)90456-x
11. Gaut JP, Liapis H. IgA dominant post-infectious glomerulonephritis: Pathology and insights into disease mechanisms. Diagn Histopathol. 2013;19:175-81. doi: 10.1016/j.mpdhp.2013.02.005
12. Kurosu A, Oka N, Hamaguchi T, Yoshikawa N, Joh K. Infantile immunoglobulin A nephropathy showing features of membranoproliferative glomerulonephritis. Tohoku J Exp Med. 2012;228:253-8. doi: 10.1620/tjem.228.253
13. Ferrario G, Palazzi P, Torri Tarelli L, Volpi A, Meroni M, Giordano F, et al. Membranoproliferative glomerulonephritis with IgA deposits in patients with alcoholic cirrhosis. Pathologica. 1986;78:469-78.
14. Trimarchi H, Barratt J, Cattran DC, Cook HT, Coppo R, Haas M, et al. Oxford Classification of IgA nephropathy 2016: an update from the IgA Nephropathy Classification Working Group. Kidney Int. 2017;91(5):1014-21. doi: 10.1016/j.kint.2017.02.003
15. [Dobronravov VA, Dunaeva NV. Renal damage and chronic hepatitis C virus. Nefrologiya. 2008;12(4):9-19 (In Russ.)]. https://cyberleninka.ru/article/n/porazhenie-pochek-i-hronicheskiy-virusnyy-gepatit-s
16. Sethi S, Zand L, Leung N, Smith RJ, Jevremonic D, Herrmann SS, Fervenza FC. Membranoproliferative glomerulonephritis secondary to monoclonal gammopathy. Clin J Am Soc Nephrol. 2010;5(5):770-82. doi: 10.2215/CJN.06760909
17. Pickering MC, D’Agati VD, Nester CM, Smith RJ, Haas M, Appel GB, et al. C3 glomerulopathy: Consensus report. Kidney Int. 2013;84:1079-89. doi: 10.1038/ki.2013.377
18. Doshi M, Lahoti A, Danesh FR, Batuman V, Sanders PW. American Society of Nephrology Onco-Nephrology Forum. Paraprotein-Related Kidney Disease: Kidney Injury from Paraproteins-What Determines the Site of Injury? Clin J Am Soc Nephrol. 2016;11(12):2288-94. doi: 10.2215/CJN.02560316
19. Foltyn Zadura A, Zipfel PF, Bokarewa MI, Sturfelt G, Jönsen A, Nilsson SC, et al. Factor H autoantibodies and deletion of Complement Factor H-Related protein-1 in rheumatic diseases in comparison to atypical hemolytic uremic syndrome. Arthritis Res Ther. 2012;14(4):R185. doi: 10.1186/ar4016
20. Iatropoulos P, Noris M, Mele C, Piras R, Valoti E, Bresin E, et al. Complement gene variants determine the risk of immunoglobulin-associated MPGN and C3 glomerulopathy and predict long-term renal outcome. Mol Immunol. 2016;71:131-42. doi: 10.1016/j.molimm.2016.01.010
21. Marinozzi MC, Roumenina LT, Chauvet S, Hertig A, Bertrand D, Olagne J, et al. Anti-Factor B and Anti-C3b Autoantibodies in C3 Glomerulopathy and Ig-Associated Membranoproliferative GN. J Am Soc Nephrol. 2017;28(5):1603-13. doi: 10.1681/ASN.2016030343
22. Iatropoulos P, Daina E, Curreri M, Piras R, Valoti E, Mele C, et al. Cluster Analysis Identifies Distinct Pathogenetic Patterns in C3 Glomerulopathies/Immune Complex-Mediated Membranoproliferative GN. J Am Soc Nephrol. 2018;29(1):283-94. doi: 10.1681/ASN.2017030258
23. Hou J, Markowitz GS, Bomback AS, Appel GB, Herlitz LC, Barry Stokes M, d'Agati VD. Toward a working definition of C3 glomerulopathy by immunofluorescence. Kidney Int. 2014;85(2):450-6. doi: 10.1038/ki.2013.340
24. [Yurova VA, Kozlovskaya NL. Membranoproliferative glomerulonephritis: a new classification and pathogenesis. Klinicheskaya Nefrologiya. 2016;(3-4):4-10 (In Russ.)]. https://nephrologyjournal.ru/ru/archive/article/33647
25. Palmer SC, Tunnicliffe DJ, Singh-Grewal D, Mavridis D, Tonelli M, Johnson DW, et al. Induction and Maintenance Immunosuppression Treatment of Proliferative Lupus Nephritis: A Network Meta-analysis of Randomized Trials. Am J Kidney Dis. 2017;70(3):324-36. doi: 10.1053/j.ajkd.2016.12.008
26. Lorenz G, Desai J, Anders HJ. Lupus nephritis: update on mechanisms of systemic autoimmunity and kidney immunopathology. Curr Opin Nephrol Hypertens. 2014;23(3):211-7. doi: 10.1097/01.mnh.0000444816.57378.21
27. Touma Z, Gladman DD. Current and future therapies for SLE: obstacles and recommendations for the development of novel treatments. Lupus Sci Med. 2017;4(1):e000239. doi: 10.1136/lupus-2017-000239
28. [Shilov EM, Bobkova IN, Kolina IB, Kamishova ES. Clinical recommendations for diagnostics and treatment of IgA-nephropathy. Nefrologiya. 2015;19(6):83-92 (In Russ.)]. http://journal.nephrolog.ru/jour/article/view/146
29. Shao X, Li B, Cao L, Liang L, Yang J, Wang Y, et al. Evaluation of crescent formation as a predictive marker in immunoglobulin A nephropathy: a systematic review and meta-analysis. Oncotarget. 2017;8(28):46436-48. doi: 10.18632/oncotarget.17502
30. Tam FWK, Pusey CD. TESTING Corticosteroids in IgA Nephropathy: A Continuing Challenge. Clin J Am Soc Nephrol. 2018;13(1):158-60. doi: 10.2215/CJN.10560917
31. Johnson RJ, Shimada M. Contemporary Management of Hepatitis C in Patients with CKD. Clin J Am Soc Nephrol. 2017;12(10):1563-5. doi: 10.2215/CJN.07620717
32. De Vita S, Quartuccio L, Isola M, Mazzaro C, Scaini P, Lenzi M, et al. A randomized controlled trial of rituximab for the treatment of severe cryoglobulinemic vasculitis. Arthritis Rheum. 2012;64(3):843-53. doi: 10.1002/art.34331
33. [Kozlovskaya LV, Rameev VV, Kogarko IN, Gordovskaya NB, Chebotareva NV, Androsova TV. Renal lesions associated with monoclonal gammopathies of undetermined significance: clinical forms, mechanisms of development, approaches to treatment. Klinicheskaya Meditsina. 2016;94(12):892-901 (In Russ.)]. doi: 10.18821/0023-2149-2016-94-12-892-901
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Научно-исследовательский институт нефрологии ФГБОУ ВО «Первый Санкт-Петербургский государственный медицинский университет им. акад. И.П. Павлова» Минздрава России, Санкт-Петербург, Россия
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V.A. Dobronravov, A.V. Smirnov
Research Institute of Nephrology, I.P. Pavlov First Saint Petersburg State Medical University of the Ministry of Health of the Russian Federation, Saint Petersburg, Russia