nidНефрология и диализNephrology and Dialysis1680-44222618-9801Российское диализное общество10.28996/2618-9801-2024-1-35-54nid-143Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESСовременные представления о патогенезе IgA нефропатииCurrent concepts of the pathogenesis IgA nephropathyЗубкинМ. Л.ZubkinM. L.m-zubkin@yandex.ruСолдатовД. А.SoldatovD. A.danil.soldatov.1996@mail.ruФроловаН. Ф.FrolovaN. F.nadiya.frolova@yandex.ruЧервинкоВ. И.ChervinkoV. I.dok534@yandex.ruКрюковЕ. В.KryukovE. V.evgeniy.md@mail.ruФедеральное бюджетное учреждение науки «Московский научно-исследовательский институт эпидемиологии и микробиологии имени Г.Н. Габричевского» Федеральной службы по надзору в сфере защиты прав потребителей и благополучия человека; Филиал федерального государственного бюджетного военного образовательного учреждения высшего образования «Военно-медицинская академия имени С.М. Кирова» Министерства обороны Российской Федерации; Государственное бюджетное учреждение здравоохранения города Москвы «Городская клиническая больница № 52 Департамента здравоохранения г. Москвы»РоссияG.N. Gabrichevsky Research Institute for Epidemiology and Microbiology; Branch of the S.M. Kirov Military Medical Academy; Moscow City Hospital No. 52Russian FederationГосударственное бюджетное учреждение здравоохранения города Москвы «Городская клиническая больница № 52 Департамента здравоохранения г. Москвы»РоссияMoscow City Hospital No. 52Russian FederationФедеральное государственного бюджетного военное образовательное учреждение высшего образования «Военно-медицинская академия имени С.М. Кирова» Министерства обороны Российской ФедерацииРоссияS.M. Kirov Military Medical AcademyRussian Federation2024210620242613554Copyright © Зубкин М.Л., Солдатов Д.А., Фролова Н.Ф., Червинко В.И., Крюков Е.В., 20242024Зубкин М.Л., Солдатов Д.А., Фролова Н.Ф., Червинко В.И., Крюков Е.В.Zubkin M.L., Soldatov D.A., Frolova N.F., Chervinko V.I., Kryukov E.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://journal.nephro.ru/jour/article/view/143

Введение: иммуноглобулин А нефропатия является самым распространенным в мире и в России первичным хроническим гломерулонефритом и одной из наиболее значимых причин развития терминальной стадии хронической болезни почек, требующей применения заместительной почечной терапии. Заболевание дебютирует у людей преимущественно молодого и трудоспособного возраста (от 20 до 40 лет), что определяет его социальную значимость. Также известно о высокой частоте рецидивов IgA нефропатии после трансплантации донорской почки. Спектр клинических проявлений и морфологической картины заболевания чрезвычайно разнообразен, варьируя от изолированного мочевого синдрома (асимптоматическая микрогематурия/протеинурия) до нефритической активности, нефротического синдрома и даже быстропрогрессирующего гломерулонефрита. Цель настоящего обзора представить современный взгляд на патогенез IgA нефропатии. Основные сведения: в настоящее время сформировалось принципиальное понимание природы этого заболевания, а также появились отдельные данные о более тонких механизмах его развития. Стало очевидным, что IgA нефропатия является аутоиммунной болезнью, в основе которой лежит образование иммунных комплексов (ИК). В роли аутоантигена выступает галактозо-дефицитный IgA1 (Gd-IgA1), образующийся в результате ослабленного гликозилирования отдельных участков шарнирной области тяжелых цепей этого иммуноглобулина. Его продукция осуществляется клетками MALT-системы (mucosa-associated lymphoid tissue), а именно лимфоидной ткани миндалин ротоглотки NALT (nasal-associated lymphoid tissue) и дистального отдела тонкого кишечника GALT (gut-associated lymphoid tissue). Однако в последние годы значительную роль в патогенезе IgA нефропатии отводят так называемой оси «кишечник-почка». ИК, связываясь с особыми рецепторами, расположенными на мезангиоцитах почечного клубочка, запускают процесс его повреждения. В представленном научном обзоре приводится информация о структуре и продукции IgA как в норме, так и в условиях, способствующих развитию патологии. Рассматриваются триггеры недогликозилирования IgA1, в частности, роль хронических заболеваний носоглотки и кишечника, значение состояния микробиоты этих отделов желудочно-кишечного тракта и пищевых антигенов. Новые данные о патогенезе IgA нефропатии лежат в основе разрабатываемых и уже апробируемых методов лечения заболевания и поэтому могут представлять интерес для клиницистов. Например, крупное международное многоцентровое рандомизированное двойное слепое плацебо-контролируемое клиническое исследование NefigArd продемонстрировало эффективность глюкокортикостероидного препарата (будесонид/Nefecon) с таргетным высвобождением в дистальном отделе тонкого кишечника при существенно меньшей частоте нежелательных явлений, свойственных системным кортикостероидам.

Introduction: immunoglobulin A (IgA) nephropathy is the most common primary chronic glomerulonephritis worldwide and in Russia. IgA nephropathy is one of the most significant causes of the development of end-stage chronic kidney disease, which requires renal replacement therapy. The disease occurs in people of predominantly young and working age (from 20 to 40 years), which determines its social significance. A high rate of relapse of IgA nephropathy after donor kidney transplantation was reported. The spectrum of clinical manifestations and morphological picture of the disease is diverse, ranging from isolated urinary syndrome (asymptomatic microhematuria/proteinuria) to nephritic activity, nephrotic syndrome, and even rapidly progressive glomerulonephritis. The review aimed to present current view on the pathogenesis of IgA nephropathy Main information: at present, a fundamental understanding of the nature of this disease has been formed, and some data have appeared on the more subtle mechanisms of its development. It has become obvious that IgA nephropathy is an autoimmune disease based on the immune complexes (IC) formation. Galactose-deficient IgA1 (Gd-IgA1) acts as an autoantigen and is formed as a result of underglycosylation in the hinge region of this immunoglobulin heavy chains. Its production is carried out by cells of the mucosa-associated lymphoid tissue, namely nasal-associated lymphoid tissue (NALT) and gut-associated lymphoid tissue (GALT). However, in recent years, the so-called “gut-kidney” axis has played a significant role in the pathogenesis of IgA nephropathy. IC, binding to special receptors located on the mesangiocytes of the renal glomerulus, trigger the process of its damage. The presented scientific review provides information on the structure and production of IgA both under normal and contributing to pathology conditions. The study examines the triggers of IgA1 underglycosylation, in particular, chronic nasopharynx and intestines diseases, the heterogeneity of the microbiota of these parts of the gastrointestinal tract, and food antigens. New data on the pathogenesis of IgA nephropathy underlie the developed and already tested methods of treating the disease and therefore may be of interest to clinicians. For example, a large international multi-center, randomized, double-blind, placebo-controlled NefigArd trial has demonstrated the effectiveness of a glucocorticoid drug (budesonide/Nefecon) with a targeted release in the ileum with a significantly lower incidence of adverse events in comparison to systemic corticosteroids.

IgA нефропатиягалактозо-дефицитный IgA1иммунные комплексытриггерыIgA nephropathygalactose-deficient IgA1immune complexestriggersReferencesSchena F.P., Nistor I. Epidemiology of IgA Nephropathy: A Global Perspective. Semin Nephrol. 2018. 38:435-442. doi: 10.1016/j.semnephrol.2018.05.013Schena F.P., Nistor I. Epidemiology of IgA Nephropathy: A Global Perspective. Semin Nephrol. 2018. 38:435-442. doi: 10.1016/j.semnephrol.2018.05.013Zhang Z., Zhang Y., Zhang H. IgA nephropathy: a Chinese perspective. Glomerular Dis. 2021. 2(1):30-41. doi: 10.1159/000520039Zhang Z., Zhang Y., Zhang H. IgA nephropathy: a Chinese perspective. Glomerular Dis. 2021. 2(1):30-41. doi: 10.1159/000520039Gharavi A.G., Yan Y., Scolari F. et al. IgA nephropathy, the most common cause of glomerulonephritis, is linked to 6q22-23. Nat Genet. 2000. 26(3):354-357. doi: 10.1038/81677Gharavi A.G., Yan Y., Scolari F. et al. IgA nephropathy, the most common cause of glomerulonephritis, is linked to 6q22-23. Nat Genet. 2000. 26(3):354-357. doi: 10.1038/81677Kerr M.A. The structure and function of human IgA. Biochem. J. 1990. 271:285-296. doi: 10.1042/bj2710285Kerr M.A. The structure and function of human IgA. Biochem. J. 1990. 271:285-296. doi: 10.1042/bj2710285Kutteh W.H., Prince S.J., Mestecky J. Tissue origins of human polymeric and monomeric IgA. J Immunol. 1982. 128(2):990-995.Kutteh W.H., Prince S.J., Mestecky J. Tissue origins of human polymeric and monomeric IgA. J Immunol. 1982. 128(2):990-995.Monteiro R.C., Van De Winkel J.G. IgA Fc receptors. Annu Rev Immunol. 2003. 21:177-204. doi: 10.1146/annurev.immunol.21.120601.141011Monteiro R.C., Van De Winkel J.G. IgA Fc receptors. Annu Rev Immunol. 2003. 21:177-204. doi: 10.1146/annurev.immunol.21.120601.141011Novak J., Julian B.A., Tomana M. et al. IgA glycosylation and IgA immune complexes in the of IgA nephropathy. Semin Nephrol. 2008. 28:78-87. doi: 10.1016/j.semnephrol.2007.10.009Novak J., Julian B.A., Tomana M. et al. IgA glycosylation and IgA immune complexes in the of IgA nephropathy. Semin Nephrol. 2008. 28:78-87. doi: 10.1016/j.semnephrol.2007.10.009Suzuki H., Kiryluk K., Novak J. et al. The pathophysiology of IgA nephropathy. J Am Soc Nephrol. 2011. 22(10):1795-1803. doi: 10.1681/ASN.2011050464Suzuki H., Kiryluk K., Novak J. et al. The pathophysiology of IgA nephropathy. J Am Soc Nephrol. 2011. 22(10):1795-1803. doi: 10.1681/ASN.2011050464Papista C., Berthelot L., Monteiro R.C. Dysfunctions of the Iga system: a common link between intestinal and renal diseases. Cell Mol Immunol. 2011. 8(2):126-34. doi: 10.1038/cmi.2010.69Papista C., Berthelot L., Monteiro R.C. Dysfunctions of the Iga system: a common link between intestinal and renal diseases. Cell Mol Immunol. 2011. 8(2):126-34. doi: 10.1038/cmi.2010.69He J.W., Zhou X.J., Lv J.C. et al. Perspectives on how mucosal immune responses, infections and gut microbiome shape IgA nephropathy and future therapies. Theranostics. 2020. 10(25):11462-11478. doi: 10.7150/thno.49778He J.W., Zhou X.J., Lv J.C. et al. Perspectives on how mucosal immune responses, infections and gut microbiome shape IgA nephropathy and future therapies. Theranostics. 2020. 10(25):11462-11478. doi: 10.7150/thno.49778Wehbi B., Oblet C., Boyer F. et al. Mesangial Deposition Can Strongly Involve Innate-Like IgA Molecules Lacking Affinity Maturation. J Am Soc Nephrol. 2019. 30(7):1238-1249. doi: 10.1681/ASN.2018111089Wehbi B., Oblet C., Boyer F. et al. Mesangial Deposition Can Strongly Involve Innate-Like IgA Molecules Lacking Affinity Maturation. J Am Soc Nephrol. 2019. 30(7):1238-1249. doi: 10.1681/ASN.2018111089Tomana M., Kulhavy R., Mestecky J. Receptor-mediated binding and uptake of immunoglobulin A by human liver. Gastroenterology. 1988. 94(3):762-770. doi: 10.1016/0016-5085(88)90252-1Tomana M., Kulhavy R., Mestecky J. Receptor-mediated binding and uptake of immunoglobulin A by human liver. Gastroenterology. 1988. 94(3):762-770. doi: 10.1016/0016-5085(88)90252-1Stockert R.J., Kressner M.S., Collins J.C. et al. IgA interaction with the asialoglycoprotein receptor. Proc Natl Acad Sci U S A. 1982. 79(20):6229-6231. doi: 10.1073/pnas.79.20.6229Stockert R.J., Kressner M.S., Collins J.C. et al. IgA interaction with the asialoglycoprotein receptor. Proc Natl Acad Sci U S A. 1982. 79(20):6229-6231. doi: 10.1073/pnas.79.20.6229Griffiss J.M., Goroff D.K. IgA blocks IgM and IgG-initiated immune lysis by separate molecular mechanisms. J Immunol. 1983. 130(6):2882-2885.Griffiss J.M., Goroff D.K. IgA blocks IgM and IgG-initiated immune lysis by separate molecular mechanisms. J Immunol. 1983. 130(6):2882-2885.Wilton J.M. Suppression by IgA of IgG-mediated phagocytosis by human polymorphonuclear leucocytes. Clin Exp Immunol. 1978. 34(3):423-428.Wilton J.M. Suppression by IgA of IgG-mediated phagocytosis by human polymorphonuclear leucocytes. Clin Exp Immunol. 1978. 34(3):423-428.Van Epps D.E., Williams R.C. Jr. Suppression of leukocyte chemotaxis by human IgA myeloma components. J Exp Med. 1976. 144(5):1227-1242. doi: 10.1084/jem.144.5.1227Van Epps D.E., Williams R.C. Jr. Suppression of leukocyte chemotaxis by human IgA myeloma components. J Exp Med. 1976. 144(5):1227-1242. doi: 10.1084/jem.144.5.1227Russell M.W., Sibley D.A., Nikolova E.B. et al. IgA antibody as a non-inflammatory regulator of immunity. Biochem. Soc. Trans. 1997. 25:466-470.Russell M.W., Sibley D.A., Nikolova E.B. et al. IgA antibody as a non-inflammatory regulator of immunity. Biochem. Soc. Trans. 1997. 25:466-470.Pasquier B., Launay P., Kanamaru Y. et al. Identification of FcalphaRI as an inhibitory receptor that controls inflammation: dual role of FcRgamma ITAM. Immunity. 2005. 22(1):31-42. doi: 10.1016/j.immuni.2004.11.017Pasquier B., Launay P., Kanamaru Y. et al. Identification of FcalphaRI as an inhibitory receptor that controls inflammation: dual role of FcRgamma ITAM. Immunity. 2005. 22(1):31-42. doi: 10.1016/j.immuni.2004.11.017Rossato E., Ben Mkaddem S., Kanamaru Y. et al. Reversal of Arthritis by Human Monomeric IgA Through the Receptor-Mediated SH2 Domain-Containing Phosphatase 1 Inhibitory Pathway. Arthritis Rheumatol. 2015. 67(7):1766-1777. doi: 10.1002/art.39142Rossato E., Ben Mkaddem S., Kanamaru Y. et al. Reversal of Arthritis by Human Monomeric IgA Through the Receptor-Mediated SH2 Domain-Containing Phosphatase 1 Inhibitory Pathway. Arthritis Rheumatol. 2015. 67(7):1766-1777. doi: 10.1002/art.39142Jacob C.M., Pastorino A.C., Fahl K. et al. Autoimmunity in IgA deficiency: revisiting the role of IgA as a silent housekeeper. J Clin Immunol. 2008. 28 Suppl 1:56-61. doi: 10.1007/s10875-007-9163-2Jacob C.M., Pastorino A.C., Fahl K. et al. Autoimmunity in IgA deficiency: revisiting the role of IgA as a silent housekeeper. J Clin Immunol. 2008. 28 Suppl 1:56-61. doi: 10.1007/s10875-007-9163-2Ammann A.J., Hong R. Selective IgA deficiency: presentation of 30 cases and a review of the literature. Medicine (Baltimore). 1971. 50(3):223-236.Ammann A.J., Hong R. Selective IgA deficiency: presentation of 30 cases and a review of the literature. Medicine (Baltimore). 1971. 50(3):223-236.Monteiro R.C. Role of IgA and IgA fc receptors in inflammation. J Clin Immunol. 2010. 30(1):1-9. doi: 10.1007/s10875-009-9338-0Monteiro R.C. Role of IgA and IgA fc receptors in inflammation. J Clin Immunol. 2010. 30(1):1-9. doi: 10.1007/s10875-009-9338-0Monteiro R.C., Rafeh D., Gleeson P.J. Is There a Role for Gut Microbiome Dysbiosis in IgA Nephropathy? Microorganisms. 2022. 10(4):683. doi: 10.3390/microorganisms10040683Monteiro R.C., Rafeh D., Gleeson P.J. Is There a Role for Gut Microbiome Dysbiosis in IgA Nephropathy? Microorganisms. 2022. 10(4):683. doi: 10.3390/microorganisms10040683Gesualdo L., Di Leo V., Coppo R. The mucosal immune system and IgA nephropathy. Semin Immunopathol. 2021. 43(5):657-668. doi: 10.1007/s00281-021-00871-yGesualdo L., Di Leo V., Coppo R. The mucosal immune system and IgA nephropathy. Semin Immunopathol. 2021. 43(5):657-668. doi: 10.1007/s00281-021-00871-yМерфи К., Уивер К. Иммунобиология по Джанвэю; пер. с англ. Под ред. Г.А. Игнатьевой, О.А. Свитич, И.Н. Дьякова. М.: Логосфера, 2020. 613-663 с.Мерфи К., Уивер К. Иммунобиология по Джанвэю; пер. с англ. Под ред. Г.А. Игнатьевой, О.А. Свитич, И.Н. Дьякова. М.: Логосфера, 2020. 613-663 с.Cerutti A. The regulation of IgA class switching. Nat Rev Immunol. 2008. 8(6):421-434. doi: 10.1038/nri2322Cerutti A. The regulation of IgA class switching. Nat Rev Immunol. 2008. 8(6):421-434. doi: 10.1038/nri2322Chen K., Magri G., Grasset E.K. et al. Rethinking mucosal antibody responses: IgM, IgG and IgD join IgA. Nat Rev Immunol. 2020. 20(7):427-441. doi: 10.1038/s41577-019-0261-1Chen K., Magri G., Grasset E.K. et al. Rethinking mucosal antibody responses: IgM, IgG and IgD join IgA. Nat Rev Immunol. 2020. 20(7):427-441. doi: 10.1038/s41577-019-0261-1Du Y., Cheng T., Liu C. et al. IgA Nephropathy: Current Understanding and Perspectives on Pathogenesis and Targeted Treatment. Diagnostics (Basel). 2023. 13(2):303. doi: 10.3390/diagnostics13020303Du Y., Cheng T., Liu C. et al. IgA Nephropathy: Current Understanding and Perspectives on Pathogenesis and Targeted Treatment. Diagnostics (Basel). 2023. 13(2):303. doi: 10.3390/diagnostics13020303Saha M.K., Julian B.A., Novak J. et al. Secondary IgA nephropathy. Kidney Int. 2018. 94:674-681. doi: 10.1016/j.kint.2018.02.030Saha M.K., Julian B.A., Novak J. et al. Secondary IgA nephropathy. Kidney Int. 2018. 94:674-681. doi: 10.1016/j.kint.2018.02.030Kaetzel C.S., Mestecky J., Johansen F.E. Two Cells, One Antibody: The Discovery of the Cellular Origins and Transport of Secretory IgA. J. Immunol. 2017. 198:1765-1767. doi: 10.4049/jimmunol.1700025Kaetzel C.S., Mestecky J., Johansen F.E. Two Cells, One Antibody: The Discovery of the Cellular Origins and Transport of Secretory IgA. J. Immunol. 2017. 198:1765-1767. doi: 10.4049/jimmunol.1700025Tuma P., Hubbard A.L. Transcytosis: crossing cellular barriers. Physiol Rev. 2003. 83:871-932. doi: 10.1152/physrev.00001.2003Tuma P., Hubbard A.L. Transcytosis: crossing cellular barriers. Physiol Rev. 2003. 83:871-932. doi: 10.1152/physrev.00001.2003Kiyono H., Fukuyama S. NALT- versus Peyer's-patch-mediated mucosal immunity. Nat Rev Immunol. 2004. 4(9):699-710. doi: 10.1038/nri1439Kiyono H., Fukuyama S. NALT- versus Peyer's-patch-mediated mucosal immunity. Nat Rev Immunol. 2004. 4(9):699-710. doi: 10.1038/nri1439Fagarasan S., Kawamoto S., Kanagawa O. et al. Adaptive immune regulation in the gut: T cell-dependent and T cell-independent IgA synthesis. Annu Rev Immunol. 2010. 28:243-273. doi: 10.1146/annurev-immunol-030409-101314Fagarasan S., Kawamoto S., Kanagawa O. et al. Adaptive immune regulation in the gut: T cell-dependent and T cell-independent IgA synthesis. Annu Rev Immunol. 2010. 28:243-273. doi: 10.1146/annurev-immunol-030409-101314Grasset E.K., Chorny A., Casas-Recasens S. et al. Gut T cell-independent IgA responses to commensal bacteria require engagement of the TACI receptor on B cells. Sci Immunol. 2020. 5(49):eaat7117. doi: 10.1126/sciimmunol.aat7117Grasset E.K., Chorny A., Casas-Recasens S. et al. Gut T cell-independent IgA responses to commensal bacteria require engagement of the TACI receptor on B cells. Sci Immunol. 2020. 5(49):eaat7117. doi: 10.1126/sciimmunol.aat7117Berger J., Hinglais N. Les ddpôts intercapillaires d'IgA-IgG [Intercapillary deposits of IgA-IgG]. J Urol Nephrol (Paris). 1968. 74(9):694-695.Berger J., Hinglais N. Les ddpôts intercapillaires d'IgA-IgG [Intercapillary deposits of IgA-IgG]. J Urol Nephrol (Paris). 1968. 74(9):694-695.Coppo R. The intestine-renal connection in IgA nephropathy. Nephrol Dial Transplant. 2015. 30(3):360-366. doi: 10.1093/ndt/gfu343Coppo R. The intestine-renal connection in IgA nephropathy. Nephrol Dial Transplant. 2015. 30(3):360-366. doi: 10.1093/ndt/gfu343Maillard N., Wyatt R.J., Julian B.A. et al. Current Understanding of the Role of Complement in IgA Nephropathy. J Am Soc Nephrol. 2015. 26(7):1503-1512. doi: 10.1681/ASN.2014101000Maillard N., Wyatt R.J., Julian B.A. et al. Current Understanding of the Role of Complement in IgA Nephropathy. J Am Soc Nephrol. 2015. 26(7):1503-1512. doi: 10.1681/ASN.2014101000Sinniah R. Occurrence of mesangial IgA and IgM deposits in a control necropsy population. J Clin Pathol. 1983. 36(3):276-279. doi: 10.1136/jcp.36.3.276Sinniah R. Occurrence of mesangial IgA and IgM deposits in a control necropsy population. J Clin Pathol. 1983. 36(3):276-279. doi: 10.1136/jcp.36.3.276Waldherr R., Rambausek M., Duncker W.D. et al. Frequency of mesangial IgA deposits in a non-selected autopsy series. Nephrol Dial Transplant. 1989. 4(11):943-946. doi: 10.1093/ndt/4.11.943Waldherr R., Rambausek M., Duncker W.D. et al. Frequency of mesangial IgA deposits in a non-selected autopsy series. Nephrol Dial Transplant. 1989. 4(11):943-946. doi: 10.1093/ndt/4.11.943Cuevas X., Lloveras J., Mir M. et al. Disappearance of mesangial IgA deposits from the kidneys of two donors after transplantation. Transplant Proc. 1987. 19(1 Pt 3):2208-2209.Cuevas X., Lloveras J., Mir M. et al. Disappearance of mesangial IgA deposits from the kidneys of two donors after transplantation. Transplant Proc. 1987. 19(1 Pt 3):2208-2209.Silva F.G., Chander P., Pirani C.L. et al. Disappearance of glomerular mesangial IgA deposits after renal allograft transplantation. Transplantation. 1982. 33(2):241-246.Silva F.G., Chander P., Pirani C.L. et al. Disappearance of glomerular mesangial IgA deposits after renal allograft transplantation. Transplantation. 1982. 33(2):241-246.Novak J., Tomana M., Matousovic K. et al. IgA1-containing immune complexes in IgA nephropathy differentially affect proliferation of mesangial cells. Kidney Int. 2005. 67(2):504-513. doi: 10.1111/j.1523-1755.2005.67107.xNovak J., Tomana M., Matousovic K. et al. IgA1-containing immune complexes in IgA nephropathy differentially affect proliferation of mesangial cells. Kidney Int. 2005. 67(2):504-513. doi: 10.1111/j.1523-1755.2005.67107.xNovak J., Raskova Kafkova L., Suzuki H. et al. IgA1 immune complexes from pediatric patients with IgA nephropathy activate cultured human mesangial cells. Nephrol Dial Transplant. 2011. 26(11):3451-3457. doi: 10.1093/ndt/gfr448Novak J., Raskova Kafkova L., Suzuki H. et al. IgA1 immune complexes from pediatric patients with IgA nephropathy activate cultured human mesangial cells. Nephrol Dial Transplant. 2011. 26(11):3451-3457. doi: 10.1093/ndt/gfr448Rifai A., Small P.A. Jr., Teague P.O. et al. Experimental IgA nephropathy. J Exp Med. 1979. 150(5):1161-1173. doi: 10.1084/jem.150.5.1161Rifai A., Small P.A. Jr., Teague P.O. et al. Experimental IgA nephropathy. J Exp Med. 1979. 150(5):1161-1173. doi: 10.1084/jem.150.5.1161Isaacs K.L., Miller F. Role of antigen size and charge in immune complex glomerulonephritis. Lab. Investig. 1982. 47:198-205.Isaacs K.L., Miller F. Role of antigen size and charge in immune complex glomerulonephritis. Lab. Investig. 1982. 47:198-205.Tomino Y., Sakai H., Miura M. et al. Detection of polymeric IgA in glomeruli from patients with IgA nephropathy. Clin. Exp. Immunol. 1982. 49:419-425.Tomino Y., Sakai H., Miura M. et al. Detection of polymeric IgA in glomeruli from patients with IgA nephropathy. Clin. Exp. Immunol. 1982. 49:419-425.Monteiro R.C., Halbwachs-Mecarelli L., Roque-Barreira M.C. et al. Charge and size of mesangial IgA in IgA nephropathy. Kidney Int. 1985. 28(4):666-671. doi: 10.1038/ki.1985.181Monteiro R.C., Halbwachs-Mecarelli L., Roque-Barreira M.C. et al. Charge and size of mesangial IgA in IgA nephropathy. Kidney Int. 1985. 28(4):666-671. doi: 10.1038/ki.1985.181Mestecky J., Tomana M., Crowley-Nowick P.A. et al. Defective galactosylation and clearance of IgA1 molecules as a possible etiopathogenic factor in IgA nephropathy. Contrib Nephrol. 1993. 104:172-182. doi: 10.1159/000422410Mestecky J., Tomana M., Crowley-Nowick P.A. et al. Defective galactosylation and clearance of IgA1 molecules as a possible etiopathogenic factor in IgA nephropathy. Contrib Nephrol. 1993. 104:172-182. doi: 10.1159/000422410Tomana M., Matousovic K., Julian B.A. et al. Galactose-deficient IgA1 in sera of IgA nephropathy patients is present in complexes with IgG. Kidney Int. 1997. 52(2):509-516. doi: 10.1038/ki.1997.361Tomana M., Matousovic K., Julian B.A. et al. Galactose-deficient IgA1 in sera of IgA nephropathy patients is present in complexes with IgG. Kidney Int. 1997. 52(2):509-516. doi: 10.1038/ki.1997.361Allen A.C., Bailey E.M., Brenchley P.E. et al. Mesangial IgA1 in IgA nephropathy exhibits aberrant O-glycosylation: observations in three patients. Kidney Int. 2001. 60(3):969-973. doi: 10.1046/j.1523-1755.2001.060003969.xAllen A.C., Bailey E.M., Brenchley P.E. et al. Mesangial IgA1 in IgA nephropathy exhibits aberrant O-glycosylation: observations in three patients. Kidney Int. 2001. 60(3):969-973. doi: 10.1046/j.1523-1755.2001.060003969.xGharavi A.G., Moldoveanu Z., Wyatt R.J. et al. Aberrant IgA1 glycosylation is inherited in familial and sporadic IgA nephropathy. J Am Soc Nephrol. 2008. 19(5):1008.Gharavi A.G., Moldoveanu Z., Wyatt R.J. et al. Aberrant IgA1 glycosylation is inherited in familial and sporadic IgA nephropathy. J Am Soc Nephrol. 2008. 19(5):1008.Wang Y.N., Zhou X.J., Chen P. et al. Interaction between GALNT12 and C1GALT1 Associates with Galactose-Deficient IgA1 and IgA Nephropathy. J Am Soc Nephrol. 2021. 32(3):545-552. doi: 10.1681/ASN.2020060823Wang Y.N., Zhou X.J., Chen P. et al. Interaction between GALNT12 and C1GALT1 Associates with Galactose-Deficient IgA1 and IgA Nephropathy. J Am Soc Nephrol. 2021. 32(3):545-552. doi: 10.1681/ASN.2020060823Serino G., Sallustio F., Cox S.N. et al. Abnormal miR-148b expression promotes aberrant glycosylation of IgA1 in IgA nephropathy. J Am Soc Nephrol. 2012. 23(5):814-824. doi: 10.1681/ASN.2011060567Serino G., Sallustio F., Cox S.N. et al. Abnormal miR-148b expression promotes aberrant glycosylation of IgA1 in IgA nephropathy. J Am Soc Nephrol. 2012. 23(5):814-824. doi: 10.1681/ASN.2011060567Qin W., Zhong X., Fan J.M. et al. External suppression causes the low expression of the Cosmc gene in IgA nephropathy. Nephrol Dial Transplant. 2008. 23(5):1608-1614. doi: 10.1093/ndt/gfm781Qin W., Zhong X., Fan J.M. et al. External suppression causes the low expression of the Cosmc gene in IgA nephropathy. Nephrol Dial Transplant. 2008. 23(5):1608-1614. doi: 10.1093/ndt/gfm781Suzuki H., Moldoveanu Z., Hall S. et al. IgA1-secreting cell lines from patients with IgA nephropathy produce aberrantly glycosylated IgA1. J Clin Invest. 2008. 118(2):629-639. doi: 10.1172/JCI33189Suzuki H., Moldoveanu Z., Hall S. et al. IgA1-secreting cell lines from patients with IgA nephropathy produce aberrantly glycosylated IgA1. J Clin Invest. 2008. 118(2):629-639. doi: 10.1172/JCI33189Bene M.C., Faure G., Duheille J. IgA nephropathy: characterization of the polymeric nature of mesangial deposits by in vitro binding of free secretory component. Clin Exp Immunol. 1982. 47(3):527-534.Bene M.C., Faure G., Duheille J. IgA nephropathy: characterization of the polymeric nature of mesangial deposits by in vitro binding of free secretory component. Clin Exp Immunol. 1982. 47(3):527-534.Knoppova B., Reily C., Maillard N. et al. The Origin and Activities of IgA1-Containing Immune Complexes in IgA Nephropathy. Front Immunol. 2016. 7:117. doi: 10.3389/fimmu.2016.00117Knoppova B., Reily C., Maillard N. et al. The Origin and Activities of IgA1-Containing Immune Complexes in IgA Nephropathy. Front Immunol. 2016. 7:117. doi: 10.3389/fimmu.2016.00117Coppo R. Treatment of IgA nephropathy: Recent advances and prospects. Nephrol Ther. 2018. 14 Suppl 1:13-21. doi: 10.1016/j.nephro.2018.02.010Coppo R. Treatment of IgA nephropathy: Recent advances and prospects. Nephrol Ther. 2018. 14 Suppl 1:13-21. doi: 10.1016/j.nephro.2018.02.010Tomana M., Novak J., Julian B.A. et al. Circulating immune complexes in IgA nephropathy consist of IgA1 with galactose-deficient hinge region and antiglycan antibodies. J Clin Invest. 1999. 104(1):73-81. doi: 10.1172/JCI5535Tomana M., Novak J., Julian B.A. et al. Circulating immune complexes in IgA nephropathy consist of IgA1 with galactose-deficient hinge region and antiglycan antibodies. J Clin Invest. 1999. 104(1):73-81. doi: 10.1172/JCI5535Rizk D.V., Saha M.K., Hall S. et al. Glomerular Immunodeposits of Patients with IgA Nephropathy Are Enriched for IgG Autoantibodies Specific for Galactose-Deficient IgA1. J Am Soc Nephrol. 2019. 30(10):2017-2026. doi: 10.1681/ASN.2018111156Rizk D.V., Saha M.K., Hall S. et al. Glomerular Immunodeposits of Patients with IgA Nephropathy Are Enriched for IgG Autoantibodies Specific for Galactose-Deficient IgA1. J Am Soc Nephrol. 2019. 30(10):2017-2026. doi: 10.1681/ASN.2018111156Mestecky J., Hashim O.H., Tomana M. Alterations in the IgA carbohydrate chains influence the cellular distribution of IgA1. Contrib Nephrol. 1995. 111:66-71. doi: 10.1159/000423879Mestecky J., Hashim O.H., Tomana M. Alterations in the IgA carbohydrate chains influence the cellular distribution of IgA1. Contrib Nephrol. 1995. 111:66-71. doi: 10.1159/000423879Novak J., Vu H.L., Novak L. et al. Interactions of human mesangial cells with IgA and IgA-containing immune complexes. Kidney Int. 2002. 62(2):465-475. doi: 10.1046/j.1523-1755.2002.00477.xNovak J., Vu H.L., Novak L. et al. Interactions of human mesangial cells with IgA and IgA-containing immune complexes. Kidney Int. 2002. 62(2):465-475. doi: 10.1046/j.1523-1755.2002.00477.xPhillips J.O., Komiyama K., Epps J.M. et al. Role of hepatocytes in the uptake of IgA and IgA-containing immune complexes in mice. Mol Immunol. 1988. 25(9):873-879. doi: 10.1016/0161-5890(88)90124-1Phillips J.O., Komiyama K., Epps J.M. et al. Role of hepatocytes in the uptake of IgA and IgA-containing immune complexes in mice. Mol Immunol. 1988. 25(9):873-879. doi: 10.1016/0161-5890(88)90124-1Launay P., Grossetête B., Arcos-Fajardo M. et al. Fcalpha receptor (CD89) mediates the development of immunoglobulin A (IgA) nephropathy (Berger's disease). Evidence for pathogenic soluble receptor-Iga complexes in patients and CD89 transgenic mice. J Exp Med. 2000. 191(11):1999-2009. doi: 10.1084/jem.191.11.1999Launay P., Grossetête B., Arcos-Fajardo M. et al. Fcalpha receptor (CD89) mediates the development of immunoglobulin A (IgA) nephropathy (Berger's disease). Evidence for pathogenic soluble receptor-Iga complexes in patients and CD89 transgenic mice. J Exp Med. 2000. 191(11):1999-2009. doi: 10.1084/jem.191.11.1999Van der Boog P.J., De Fijter J.W., Van Kooten C. et al. Complexes of IgA with FcalphaRI/CD89 are not specific for primary IgA nephropathy. Kidney Int. 2003. 63(2):514-521. doi: 10.1046/j.1523-1755.2003.00756.xVan der Boog P.J., De Fijter J.W., Van Kooten C. et al. Complexes of IgA with FcalphaRI/CD89 are not specific for primary IgA nephropathy. Kidney Int. 2003. 63(2):514-521. doi: 10.1046/j.1523-1755.2003.00756.xVuong M.T., Hahn-Zoric M., Lundberg S. et al. Association of soluble CD89 levels with disease progression but not susceptibility in IgA nephropathy. Kidney Int. 2010. 78(12):1281-1287. doi: 10.1038/ki.2010.314Vuong M.T., Hahn-Zoric M., Lundberg S. et al. Association of soluble CD89 levels with disease progression but not susceptibility in IgA nephropathy. Kidney Int. 2010. 78(12):1281-1287. doi: 10.1038/ki.2010.314Berthelot L., Robert T., Vuiblet V. et al. Recurrent IgA nephropathy is predicted by altered glycosylated IgA, autoantibodies and soluble CD89 complexes. Kidney Int. 2015. 88(4):815-822. doi: 10.1038/ki.2015.158Berthelot L., Robert T., Vuiblet V. et al. Recurrent IgA nephropathy is predicted by altered glycosylated IgA, autoantibodies and soluble CD89 complexes. Kidney Int. 2015. 88(4):815-822. doi: 10.1038/ki.2015.158Cambier A., Gleeson P.J., Abbad L. et al. Soluble CD89 is a critical factor for mesangial proliferation in childhood IgA nephropathy. Kidney Int. 2022. 101(2):274-287. doi: 10.1016/j.kint.2021.09.023Cambier A., Gleeson P.J., Abbad L. et al. Soluble CD89 is a critical factor for mesangial proliferation in childhood IgA nephropathy. Kidney Int. 2022. 101(2):274-287. doi: 10.1016/j.kint.2021.09.023Boyd J.K., Barratt J. Immune complex formation in IgA nephropathy: CD89 a 'saint' or a 'sinner'? Kidney Int. 2010. 78(12):1211-1213. doi: 10.1038/ki.2010.365Boyd J.K., Barratt J. Immune complex formation in IgA nephropathy: CD89 a 'saint' or a 'sinner'? Kidney Int. 2010. 78(12):1211-1213. doi: 10.1038/ki.2010.365Xie X., Gao L., Liu P. et al. Propensity of IgA to self-aggregate via tailpiece cysteine-471 and treatment of IgA nephropathy using cysteamine. JCI Insight. 2021. 6(19):e150551. doi: 10.1172/jci.insight.150551Xie X., Gao L., Liu P. et al. Propensity of IgA to self-aggregate via tailpiece cysteine-471 and treatment of IgA nephropathy using cysteamine. JCI Insight. 2021. 6(19):e150551. doi: 10.1172/jci.insight.150551Nihei Y., Suzuki H., Suzuki Y. Current understanding of IgA antibodies in the pathogenesis of IgA nephropathy. Front Immunol. 2023. 14:1165394. doi: 10.3389/fimmu.2023.1165394Nihei Y., Suzuki H., Suzuki Y. Current understanding of IgA antibodies in the pathogenesis of IgA nephropathy. Front Immunol. 2023. 14:1165394. doi: 10.3389/fimmu.2023.1165394Гуляев С.В., Стрижаков Л.А., Чеботарева Н.В., и соавт. Роль MALT-системы кишечника в патогенезе IgA-нефропатии. Терапевтический архив. 2021. 93(6):724-728. doi: 10.26442/00403660.2021.06.200868Гуляев С.В., Стрижаков Л.А., Чеботарева Н.В., и соавт. Роль MALT-системы кишечника в патогенезе IgA-нефропатии. Терапевтический архив. 2021. 93(6):724-728. doi: 10.26442/00403660.2021.06.200868Luvizotto M.J., Menezes-Silva L., Woronik V. et al. Gut-kidney axis in IgA nephropathy: Role on mesangial cell metabolism and inflammation. Frontiers in Cell and Developmental Biology. 2022. 10:993716. doi: 10.3389/fcell.2022.993716Luvizotto M.J., Menezes-Silva L., Woronik V. et al. Gut-kidney axis in IgA nephropathy: Role on mesangial cell metabolism and inflammation. Frontiers in Cell and Developmental Biology. 2022. 10:993716. doi: 10.3389/fcell.2022.993716Moura I.C., Centelles M.N., Arcos-Fajardo M. et al. Identification of the transferrin receptor as a novel immunoglobulin (Ig)A1 receptor and its enhanced expression on mesangial cells in IgA nephropathy. J Exp Med. 2001. 194(4):417-425. doi: 10.1084/jem.194.4.417Moura I.C., Centelles M.N., Arcos-Fajardo M. et al. Identification of the transferrin receptor as a novel immunoglobulin (Ig)A1 receptor and its enhanced expression on mesangial cells in IgA nephropathy. J Exp Med. 2001. 194(4):417-425. doi: 10.1084/jem.194.4.417Moura I.C., Arcos-Fajardo M., Sadaka C. et al. Glycosylation and size of IgA1 are essential for interaction with mesangial transferrin receptor in IgA nephropathy. J Am Soc Nephrol. 2004. 15(3):622-634. doi: 10.1097/01.asn.0000115401.07980.0cMoura I.C., Arcos-Fajardo M., Sadaka C. et al. Glycosylation and size of IgA1 are essential for interaction with mesangial transferrin receptor in IgA nephropathy. J Am Soc Nephrol. 2004. 15(3):622-634. doi: 10.1097/01.asn.0000115401.07980.0cMoura I.C., Arcos-Fajardo M., Gdoura A. et al. Engagement of transferrin receptor by polymeric IgA1: evidence for a positive feedback loop involving increased receptor expression and mesangial cell proliferation in IgA nephropathy. J Am Soc Nephrol. 2005. 16(9):2667-2676. doi: 10.1681/ASN.2004111006Moura I.C., Arcos-Fajardo M., Gdoura A. et al. Engagement of transferrin receptor by polymeric IgA1: evidence for a positive feedback loop involving increased receptor expression and mesangial cell proliferation in IgA nephropathy. J Am Soc Nephrol. 2005. 16(9):2667-2676. doi: 10.1681/ASN.2004111006Jhee J.H., Nam B.Y., Park J.T. et al. CD71 mesangial IgA1 receptor and the progression of IgA nephropathy. Transl Res. 2021. 230:34-43. doi: 10.1016/j.trsl.2020.10.007Jhee J.H., Nam B.Y., Park J.T. et al. CD71 mesangial IgA1 receptor and the progression of IgA nephropathy. Transl Res. 2021. 230:34-43. doi: 10.1016/j.trsl.2020.10.007Gómez-Guerrero C., Duque N., Egido J. Stimulation of Fc(alpha) receptors induces tyrosine phosphorylation of phospholipase C-gamma(1), phosphatidylinositol phosphate hydrolysis, and Ca2+ mobilization in rat and human mesangial cells. J Immunol. 1996. 156(11):4369-76.Gómez-Guerrero C., Duque N., Egido J. Stimulation of Fc(alpha) receptors induces tyrosine phosphorylation of phospholipase C-gamma(1), phosphatidylinositol phosphate hydrolysis, and Ca2+ mobilization in rat and human mesangial cells. J Immunol. 1996. 156(11):4369-76.Gómez-Guerrero C., López-Armada M.J., González E. et al. Soluble IgA and IgG aggregates are catabolized by cultured rat mesangial cells and induce production of TNF-alpha and IL-6, and proliferation. J Immunol. 1994. 153(11):5247-55.Gómez-Guerrero C., López-Armada M.J., González E. et al. Soluble IgA and IgG aggregates are catabolized by cultured rat mesangial cells and induce production of TNF-alpha and IL-6, and proliferation. J Immunol. 1994. 153(11):5247-55.Boyd J.K., Cheung C.K., Molyneux K. et al. An update on the pathogenesis and treatment of IgA nephropathy. Kidney Int. 2012. 81(9):833-843. doi: 10.1038/ki.2011.501Boyd J.K., Cheung C.K., Molyneux K. et al. An update on the pathogenesis and treatment of IgA nephropathy. Kidney Int. 2012. 81(9):833-843. doi: 10.1038/ki.2011.501Monteiro R.C. Recent advances in the physiopathology of IgA nephropathy. Nephrol Ther. 2018. 14 Suppl 1:1-8. doi: 10.1016/j.nephro.2018.02.004Monteiro R.C. Recent advances in the physiopathology of IgA nephropathy. Nephrol Ther. 2018. 14 Suppl 1:1-8. doi: 10.1016/j.nephro.2018.02.004Berthelot L., Papista C., Maciel T.T. et al. Transglutaminase is essential for IgA nephropathy development acting through IgA receptors. J Exp Med. 2012. 209:793-806. doi: 10.1084/jem.20112005Berthelot L., Papista C., Maciel T.T. et al. Transglutaminase is essential for IgA nephropathy development acting through IgA receptors. J Exp Med. 2012. 209:793-806. doi: 10.1084/jem.20112005Ikee R., Kobayashi S., Hemmi N. et al. Involvement of transglutaminase-2 in pathological changes in renal disease. Nephron Clin Pract. 2007. 105:139-146. doi: 10.1159/000098646Ikee R., Kobayashi S., Hemmi N. et al. Involvement of transglutaminase-2 in pathological changes in renal disease. Nephron Clin Pract. 2007. 105:139-146. doi: 10.1159/000098646Berger J. IgA glomerular deposits in renal disease. Transplant Proc. 1969. 1(4):939-944.Berger J. IgA glomerular deposits in renal disease. Transplant Proc. 1969. 1(4):939-944.Béné M.C., Faure G.C. Mucosal immunity and IgA nephropathies. Semin Nephrol. 1987. 7(4):297-300.Béné M.C., Faure G.C. Mucosal immunity and IgA nephropathies. Semin Nephrol. 1987. 7(4):297-300.Wyatt R.J., Kanayama Y., Julian B.A. et al. Complement activation in IgA nephropathy. Kidney Int. 1987. 31(4):1019-1023. doi: 10.1038/ki.1987.101Wyatt R.J., Kanayama Y., Julian B.A. et al. Complement activation in IgA nephropathy. Kidney Int. 1987. 31(4):1019-1023. doi: 10.1038/ki.1987.101Bene M.C., Faure G.C. Composition of mesangial deposits in IgA nephropathy: complement factors. Nephron. 1987. 46(2):219. doi: 10.1159/000184350Bene M.C., Faure G.C. Composition of mesangial deposits in IgA nephropathy: complement factors. Nephron. 1987. 46(2):219. doi: 10.1159/000184350Evans D.J., Williams D.G., Peters D.K. et al. Glomerular deposition of properdin in Henoch-Schönlein syndrome and idiopathic focal nephritis. Br Med J. 1973. 3(5875):326-328. doi: 10.1136/bmj.3.5875.326Evans D.J., Williams D.G., Peters D.K. et al. Glomerular deposition of properdin in Henoch-Schönlein syndrome and idiopathic focal nephritis. Br Med J. 1973. 3(5875):326-328. doi: 10.1136/bmj.3.5875.326Zhang J.J., Jiang L., Liu G. et al. Levels of urinary complement factor H in patients with IgA nephropathy are closely associated with disease activity. Scand J Immunol. 2009. 69(5):457-464. doi: 10.1111/j.1365-3083.2009.02234.xZhang J.J., Jiang L., Liu G. et al. Levels of urinary complement factor H in patients with IgA nephropathy are closely associated with disease activity. Scand J Immunol. 2009. 69(5):457-464. doi: 10.1111/j.1365-3083.2009.02234.xMurphy B., Georgiou T., Machet D. et al. Factor H-related protein-5: a novel component of human glomerular immune deposits. Am J Kidney Dis. 2002. 39(1):24-27. doi: 10.1053/ajkd.2002.29873Murphy B., Georgiou T., Machet D. et al. Factor H-related protein-5: a novel component of human glomerular immune deposits. Am J Kidney Dis. 2002. 39(1):24-27. doi: 10.1053/ajkd.2002.29873Roos A., Bouwman L.H., van Gijlswijk-Janssen D.J. et al. Human IgA activates the complement system via the mannan-binding lectin pathway. J Immunol. 2001. 167(5):2861-2868. doi: 10.4049/jimmunol.167.5.2861Roos A., Bouwman L.H., van Gijlswijk-Janssen D.J. et al. Human IgA activates the complement system via the mannan-binding lectin pathway. J Immunol. 2001. 167(5):2861-2868. doi: 10.4049/jimmunol.167.5.2861Endo M., Ohi H., Ohsawa I. et al. Glomerular deposition of mannose-binding lectin (MBL) indicates a novel mechanism of complement activation in IgA nephropathy. Nephrol Dial Transplant. 1998. 13(8):1984-1990. doi: 10.1093/ndt/13.8.1984Endo M., Ohi H., Ohsawa I. et al. Glomerular deposition of mannose-binding lectin (MBL) indicates a novel mechanism of complement activation in IgA nephropathy. Nephrol Dial Transplant. 1998. 13(8):1984-1990. doi: 10.1093/ndt/13.8.1984Matsuda M., Shikata K., Wada J. et al. Deposition of mannan binding protein and mannan binding protein-mediated complement activation in the glomeruli of patients with IgA nephropathy. Nephron. 1998. 80(4):408-413. doi: 10.1159/000045212Matsuda M., Shikata K., Wada J. et al. Deposition of mannan binding protein and mannan binding protein-mediated complement activation in the glomeruli of patients with IgA nephropathy. Nephron. 1998. 80(4):408-413. doi: 10.1159/000045212Roos A., Rastaldi M.P., Calvaresi N. et al. Glomerular activation of the lectin pathway of complement in IgA nephropathy is associated with more severe renal disease. J Am Soc Nephrol. 2006. 17(6):1724-1734. doi: 10.1681/ASN.2005090923Roos A., Rastaldi M.P., Calvaresi N. et al. Glomerular activation of the lectin pathway of complement in IgA nephropathy is associated with more severe renal disease. J Am Soc Nephrol. 2006. 17(6):1724-1734. doi: 10.1681/ASN.2005090923Miyazaki R., Kuroda M., Akiyama T. et al. Glomerular deposition and serum levels of complement control proteins in patients with IgA nephropathy. Clin Nephrol. 1984. 21(6):335-340.Miyazaki R., Kuroda M., Akiyama T. et al. Glomerular deposition and serum levels of complement control proteins in patients with IgA nephropathy. Clin Nephrol. 1984. 21(6):335-340.Wan J.X., Fukuda N., Endo M. et al. Complement 3 is involved in changing the phenotype of human glomerular mesangial cells. J Cell Physiol. 2007. 213(2):495-501. doi: 10.1002/jcp.21129Wan J.X., Fukuda N., Endo M. et al. Complement 3 is involved in changing the phenotype of human glomerular mesangial cells. J Cell Physiol. 2007. 213(2):495-501. doi: 10.1002/jcp.21129Nakamura T., Ebihara I., Shirato I. et al. Endothelin-1 mRNA expression by peripheral blood monocytes in IgA nephropathy. Lancet. 1993. 342(8880):1147-1148. doi: 10.1016/0140-6736(93)92126-eNakamura T., Ebihara I., Shirato I. et al. Endothelin-1 mRNA expression by peripheral blood monocytes in IgA nephropathy. Lancet. 1993. 342(8880):1147-1148. doi: 10.1016/0140-6736(93)92126-eBarton M., Yanagisawa M. Endothelin: 20 years from discovery to therapy. Can J Physiol Pharmacol. 2008. 86(8):485-498. doi: 10.1139/Y08-059Barton M., Yanagisawa M. Endothelin: 20 years from discovery to therapy. Can J Physiol Pharmacol. 2008. 86(8):485-498. doi: 10.1139/Y08-059Kohan D.E, Barton M. Endothelin and endothelin antagonists in chronic kidney disease. Kidney Int. 2014. 86(5):896-904. doi: 10.1038/ki.2014.143Kohan D.E, Barton M. Endothelin and endothelin antagonists in chronic kidney disease. Kidney Int. 2014. 86(5):896-904. doi: 10.1038/ki.2014.143Trimarchi H., Barratt J., Cattran D.C. et al. Oxford Classification of IgA nephropathy 2016: an update from the IgA Nephropathy Classification Working Group. Kidney Int. 2017. 91(5):1014-1021. doi: 10.1016/j.kint.2017.02.003Trimarchi H., Barratt J., Cattran D.C. et al. Oxford Classification of IgA nephropathy 2016: an update from the IgA Nephropathy Classification Working Group. Kidney Int. 2017. 91(5):1014-1021. doi: 10.1016/j.kint.2017.02.003Trimarchi H., Haas M., Coppo R. Crescents and IgA Nephropathy: A Delicate Marriage. J Clin Med. 2022. 11(13):3569. doi: 10.3390/jcm11133569Trimarchi H., Haas M., Coppo R. Crescents and IgA Nephropathy: A Delicate Marriage. J Clin Med. 2022. 11(13):3569. doi: 10.3390/jcm11133569Tomino Y., Yagame M., Omata F. et al. A case of IgA nephropathy associated with adeno- and herpes simplex viruses. Nephron. 1987. 47(4):258-261. doi: 10.1159/000184520Tomino Y., Yagame M., Omata F. et al. A case of IgA nephropathy associated with adeno- and herpes simplex viruses. Nephron. 1987. 47(4):258-261. doi: 10.1159/000184520Iwama H., Horikoshi S., Shirato I. et al. Epstein-Barr virus detection in kidney biopsy specimens correlates with glomerular mesangial injury. Am J Kidney Dis. 1998. 32(5):785-93. doi: 10.1016/s0272-6386(98)70134-9Iwama H., Horikoshi S., Shirato I. et al. Epstein-Barr virus detection in kidney biopsy specimens correlates with glomerular mesangial injury. Am J Kidney Dis. 1998. 32(5):785-93. doi: 10.1016/s0272-6386(98)70134-9Park J.S., Song J.H., Yang W.S. et al. Cytomegalovirus is not specifically associated with immunoglobulin A nephropathy. J Am Soc Nephrol. 1994. 4:1623-1626. doi: 10.1681/ASN.V481623Park J.S., Song J.H., Yang W.S. et al. Cytomegalovirus is not specifically associated with immunoglobulin A nephropathy. J Am Soc Nephrol. 1994. 4:1623-1626. doi: 10.1681/ASN.V481623Sharmin S., Shimizu Y., Hagiwara M. et al. Staphylococcus aureus antigens induce IgA-type glomerulonephritis in Balb/c mice. J Nephrol. 2004. 17(4):504-511.Sharmin S., Shimizu Y., Hagiwara M. et al. Staphylococcus aureus antigens induce IgA-type glomerulonephritis in Balb/c mice. J Nephrol. 2004. 17(4):504-511.Suzuki S., Nakatomi Y., Sato H. et al. Haemophilus parainfluenzae antigen and antibody in renal biopsy samples and serum of patients with IgA nephropathy. Lancet. 1994. 343(8888):12-16. doi: 10.1016/s0140-6736(94)90875-3Suzuki S., Nakatomi Y., Sato H. et al. Haemophilus parainfluenzae antigen and antibody in renal biopsy samples and serum of patients with IgA nephropathy. Lancet. 1994. 343(8888):12-16. doi: 10.1016/s0140-6736(94)90875-3Suzuki S., Kimura H., Gejyo F. [Haemophilus parainfluenzae antigens in IgA nephropathy]. Rinsho Byori. 1998. 46(1):17-25.Suzuki S., Kimura H., Gejyo F. [Haemophilus parainfluenzae antigens in IgA nephropathy]. Rinsho Byori. 1998. 46(1):17-25.Ogura Y., Suzuki S., Shirakawa T. et al. Haemophilus parainfluenzae antigen and antibody in children with IgA nephropathy and Henoch-Schönlein nephritis. Am J Kidney Dis. 2000. 36(1):47-52. doi: 10.1053/ajkd.2000.8264Ogura Y., Suzuki S., Shirakawa T. et al. Haemophilus parainfluenzae antigen and antibody in children with IgA nephropathy and Henoch-Schönlein nephritis. Am J Kidney Dis. 2000. 36(1):47-52. doi: 10.1053/ajkd.2000.8264Koyama A., Sharmin S., Sakurai H. et al. Staphylococcus aureus cell envelope antigen is a new candidate for the induction of IgA nephropathy. Kidney Int. 2004. 66(1):121-132. doi: 10.1111/j.1523-1755.2004.00714.xKoyama A., Sharmin S., Sakurai H. et al. Staphylococcus aureus cell envelope antigen is a new candidate for the induction of IgA nephropathy. Kidney Int. 2004. 66(1):121-132. doi: 10.1111/j.1523-1755.2004.00714.xTakayasu M., Hirayama K., Shimohata H. et al. Staphylococcus aureus Infection-Related Glomerulonephritis with Dominant IgA Deposition. Int J Mol Sci. 2022. 23(13):7482. doi: 10.3390/ijms23137482Takayasu M., Hirayama K., Shimohata H. et al. Staphylococcus aureus Infection-Related Glomerulonephritis with Dominant IgA Deposition. Int J Mol Sci. 2022. 23(13):7482. doi: 10.3390/ijms23137482Sethi S., De Vriese A.S., Fervenza F.C. Acute glomerulonephritis. Lancet. 2022. 399(10335):1646-1663. doi: 10.1016/S0140-6736(22)00461-5Sethi S., De Vriese A.S., Fervenza F.C. Acute glomerulonephritis. Lancet. 2022. 399(10335):1646-1663. doi: 10.1016/S0140-6736(22)00461-5Suwarti S., Yamazaki T., Svetlana C. et al. Recognition of CpG oligodeoxynucleotides by human Toll-like receptor 9 and subsequent cytokine induction. Biochem Biophys Res Commun. 2013. 430(4):1234-1239. doi: 10.1016/j.bbrc.2012.12.068Suwarti S., Yamazaki T., Svetlana C. et al. Recognition of CpG oligodeoxynucleotides by human Toll-like receptor 9 and subsequent cytokine induction. Biochem Biophys Res Commun. 2013. 430(4):1234-1239. doi: 10.1016/j.bbrc.2012.12.068Goto T., Bandoh N., Yoshizaki T. et al. Increase in B-cell-activation factor (BAFF) and IFN-gamma productions by tonsillar mononuclear cells stimulated with deoxycytidyl-deoxyguanosine oligodeoxynucleotides (CpG-ODN) in patients with IgA nephropathy. Clin Immunol. 2008. 126(3):260-269. doi: 10.1016/j.clim.2007.11.003Goto T., Bandoh N., Yoshizaki T. et al. Increase in B-cell-activation factor (BAFF) and IFN-gamma productions by tonsillar mononuclear cells stimulated with deoxycytidyl-deoxyguanosine oligodeoxynucleotides (CpG-ODN) in patients with IgA nephropathy. Clin Immunol. 2008. 126(3):260-269. doi: 10.1016/j.clim.2007.11.003Takahara M., Kumai T., Komabayashi Y. et al. Aberrant expression of APRIL (a proliferation-inducing ligand) in tonsils from IgA nephropathy patients. J Immunol Allergo Otolaryngol. 2013. 31(2):57-58.Takahara M., Kumai T., Komabayashi Y. et al. Aberrant expression of APRIL (a proliferation-inducing ligand) in tonsils from IgA nephropathy patients. J Immunol Allergo Otolaryngol. 2013. 31(2):57-58.Harabuchi Y., Takahara M. Recent advances in the immunological understanding of association between tonsil and immunoglobulin A nephropathy as a tonsil-induced autoimmune/inflammatory syndrome. Immun Inflamm Dis. 2019. 7(2):86-93. doi: 10.1002/iid3.248Harabuchi Y., Takahara M. Recent advances in the immunological understanding of association between tonsil and immunoglobulin A nephropathy as a tonsil-induced autoimmune/inflammatory syndrome. Immun Inflamm Dis. 2019. 7(2):86-93. doi: 10.1002/iid3.248Zhai Y.L., Zhu L., Shi S.F. et al. Increased APRIL Expression Induces IgA1 Aberrant Glycosylation in IgA Nephropathy. Medicine (Baltimore). 2016. 95(11):e3099. doi: 10.1097/MD.0000000000003099Zhai Y.L., Zhu L., Shi S.F. et al. Increased APRIL Expression Induces IgA1 Aberrant Glycosylation in IgA Nephropathy. Medicine (Baltimore). 2016. 95(11):e3099. doi: 10.1097/MD.0000000000003099Suzuki H., Suzuki Y., Narita I. et al. Toll-like receptor 9 affects severity of IgA nephropathy. J Am Soc Nephrol. 2008. 19(12):2384-2395. doi: 10.1681/ASN.2007121311Suzuki H., Suzuki Y., Narita I. et al. Toll-like receptor 9 affects severity of IgA nephropathy. J Am Soc Nephrol. 2008. 19(12):2384-2395. doi: 10.1681/ASN.2007121311Nozawa H., Takahara M., Yoshizaki T. et al. Selective expansion of T cell receptor (TCR) V beta 6 in tonsillar and peripheral blood T cells and its induction by in vitro stimulation with Haemophilus parainfluenzae in patients with IgA nephropathy. Clin Exp Immunol. 2008. 151(1):25-33. doi: 10.1111/j.1365-2249.2007.03523.xNozawa H., Takahara M., Yoshizaki T. et al. Selective expansion of T cell receptor (TCR) V beta 6 in tonsillar and peripheral blood T cells and its induction by in vitro stimulation with Haemophilus parainfluenzae in patients with IgA nephropathy. Clin Exp Immunol. 2008. 151(1):25-33. doi: 10.1111/j.1365-2249.2007.03523.xSegerer S., Banas B., Wörnle M. et al. CXCR3 is involved in tubulointerstitial injury in human glomerulonephritis. Am J Pathol. 2004. 164(2):635-49. doi: 10.1016/S0002-9440(10)63152-5Segerer S., Banas B., Wörnle M. et al. CXCR3 is involved in tubulointerstitial injury in human glomerulonephritis. Am J Pathol. 2004. 164(2):635-49. doi: 10.1016/S0002-9440(10)63152-5Takahara M., Komabayashi Y., Nagato T. et al. Expression of APRIL and CXCR3 in tonsils from IgA nephropathy patients. J Immunol Allergo Otolaryngol. 2012. 30(2):109-110.Takahara M., Komabayashi Y., Nagato T. et al. Expression of APRIL and CXCR3 in tonsils from IgA nephropathy patients. J Immunol Allergo Otolaryngol. 2012. 30(2):109-110.Imai T., Hieshima K., Haskell C. et al. Identification and molecular characterization of fractalkine receptor CX3CR1, which mediates both leukocyte migration and adhesion. Cell. 1997. 91(4):521-530. doi: 10.1016/s0092-8674(00)80438-9Imai T., Hieshima K., Haskell C. et al. Identification and molecular characterization of fractalkine receptor CX3CR1, which mediates both leukocyte migration and adhesion. Cell. 1997. 91(4):521-530. doi: 10.1016/s0092-8674(00)80438-9Otaka R., Takahara M., Ueda S. et al. Up-regulation of CX3CR1 on tonsillar CD8-positive cells in patients with IgA nephropathy. Hum Immunol. 2017. 78(4):375-383. doi: 10.1016/j.humimm.2017.02.004Otaka R., Takahara M., Ueda S. et al. Up-regulation of CX3CR1 on tonsillar CD8-positive cells in patients with IgA nephropathy. Hum Immunol. 2017. 78(4):375-383. doi: 10.1016/j.humimm.2017.02.004Rehnberg J., Symreng A., Ludvigsson J.F. et al. Inflammatory Bowel Disease Is More Common in Patients with IgA Nephropathy and Predicts Progression of ESKD: A Swedish Population-Based Cohort Study. J Am Soc Nephrol. 2021. 32(2):411-423. doi: 10.1681/ASN.2020060848Rehnberg J., Symreng A., Ludvigsson J.F. et al. Inflammatory Bowel Disease Is More Common in Patients with IgA Nephropathy and Predicts Progression of ESKD: A Swedish Population-Based Cohort Study. J Am Soc Nephrol. 2021. 32(2):411-423. doi: 10.1681/ASN.2020060848Barratt J., Lafayette R., Kristensen J. et al. NefIgArd Trial Investigators. Results from part A of the multi-center, double-blind, randomized, placebo-controlled NefIgArd trial, which evaluated targeted-release formulation of budesonide for the treatment of primary immunoglobulin A nephropathy. Kidney Int. 2023. 103(2):391-402. doi: 10.1016/j.kint.2022.09.017Barratt J., Lafayette R., Kristensen J. et al. NefIgArd Trial Investigators. Results from part A of the multi-center, double-blind, randomized, placebo-controlled NefIgArd trial, which evaluated targeted-release formulation of budesonide for the treatment of primary immunoglobulin A nephropathy. Kidney Int. 2023. 103(2):391-402. doi: 10.1016/j.kint.2022.09.017Davin J.C., Forget P., Mahieu P.R. Increased intestinal permeability to (51 Cr) EDTA is correlated with IgA immune complex-plasma levels in children with IgA-associated nephropathies. Acta Paediatr Scand. 1988. 77(1):118-124. doi: 10.1111/j.1651-2227.1988.tb10609.xDavin J.C., Forget P., Mahieu P.R. Increased intestinal permeability to (51 Cr) EDTA is correlated with IgA immune complex-plasma levels in children with IgA-associated nephropathies. Acta Paediatr Scand. 1988. 77(1):118-124. doi: 10.1111/j.1651-2227.1988.tb10609.xKovács T., Kun L., Schmelczer M. et al. Do intestinal hyperpermeability and the related food antigens play a role in the progression of IgA nephropathy? I. Study of intestinal permeability. Am J Nephrol. 1996. 16(6):500-505. doi: 10.1159/000169050Kovács T., Kun L., Schmelczer M. et al. Do intestinal hyperpermeability and the related food antigens play a role in the progression of IgA nephropathy? I. Study of intestinal permeability. Am J Nephrol. 1996. 16(6):500-505. doi: 10.1159/000169050Rollino C., Vischini G., Coppo R. IgA nephropathy and infections. J Nephrol. 2016. 29(4):463-468. doi: 10.1007/s40620-016-0265-xRollino C., Vischini G., Coppo R. IgA nephropathy and infections. J Nephrol. 2016. 29(4):463-468. doi: 10.1007/s40620-016-0265-xKiryluk K., Novak J. The genetics and immunobiology of IgA nephropathy. J Clin Invest. 2014. 124(6):2325-2332. doi: 10.1172/JCI74475Kiryluk K., Novak J. The genetics and immunobiology of IgA nephropathy. J Clin Invest. 2014. 124(6):2325-2332. doi: 10.1172/JCI74475Stecher B., Maier L., Hardt W.D. 'Blooming' in the gut: how dysbiosis might contribute to pathogen evolution. Nat Rev Microbiol. 2013. 11(4):277-284. doi: 10.1038/nrmicro2989Stecher B., Maier L., Hardt W.D. 'Blooming' in the gut: how dysbiosis might contribute to pathogen evolution. Nat Rev Microbiol. 2013. 11(4):277-284. doi: 10.1038/nrmicro2989Currie E.G., Coburn B., Porfilio E.A. et al. Immunoglobulin A nephropathy is characterized by anticommensal humoral immune responses. JCI Insight. 2022. 7(5):e141289. doi: 10.1172/jci.insight.141289Currie E.G., Coburn B., Porfilio E.A. et al. Immunoglobulin A nephropathy is characterized by anticommensal humoral immune responses. JCI Insight. 2022. 7(5):e141289. doi: 10.1172/jci.insight.141289He J.W., Zhou X.J., Hou P. et al. Potential Roles of Oral Microbiota in the Pathogenesis of Immunoglobin A Nephropathy. Front Cell Infect Microbiol. 2021. 11:652837. doi: 10.3389/fcimb.2021.652837He J.W., Zhou X.J., Hou P. et al. Potential Roles of Oral Microbiota in the Pathogenesis of Immunoglobin A Nephropathy. Front Cell Infect Microbiol. 2021. 11:652837. doi: 10.3389/fcimb.2021.652837Cao Y., Qiao M., Tian Z. et al. Comparative Analyses of Subgingival Microbiome in Chronic Periodontitis Patients with and Without IgA Nephropathy by High Throughput 16S rRNA Sequencing. Cell Physiol Biochem. 2018. 47(2):774-783. doi: 10.1159/000490029Cao Y., Qiao M., Tian Z. et al. Comparative Analyses of Subgingival Microbiome in Chronic Periodontitis Patients with and Without IgA Nephropathy by High Throughput 16S rRNA Sequencing. Cell Physiol Biochem. 2018. 47(2):774-783. doi: 10.1159/000490029Park J.I., Kim T.Y., Oh B. et al. Comparative analysis of the tonsillar microbiota in IgA nephropathy and other glomerular diseases. Sci Rep. 2020. 10(1):16206. doi: 10.1038/s41598-020-73035-xPark J.I., Kim T.Y., Oh B. et al. Comparative analysis of the tonsillar microbiota in IgA nephropathy and other glomerular diseases. Sci Rep. 2020. 10(1):16206. doi: 10.1038/s41598-020-73035-xChemouny J.M., Gleeson P.J., Abbad L. et al. Modulation of the microbiota by oral antibiotics treats immunoglobulin A nephropathy in humanized mice. Nephrol Dial Transplant. 2019. 34(7):1135-1144. doi: 10.1093/ndt/gfy323Chemouny J.M., Gleeson P.J., Abbad L. et al. Modulation of the microbiota by oral antibiotics treats immunoglobulin A nephropathy in humanized mice. Nephrol Dial Transplant. 2019. 34(7):1135-1144. doi: 10.1093/ndt/gfy323Nakawesi J., This S., Hütter J. et al. αvβ8 integrin-expression by BATF3-dependent dendritic cells facilitates early IgA responses to Rotavirus. Mucosal Immunol. 2021. 14(1):53-67. doi: 10.1038/s41385-020-0276-8Nakawesi J., This S., Hütter J. et al. αvβ8 integrin-expression by BATF3-dependent dendritic cells facilitates early IgA responses to Rotavirus. Mucosal Immunol. 2021. 14(1):53-67. doi: 10.1038/s41385-020-0276-8McCarthy D.D., Kujawa J., Wilson C. et al. Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy. J Clin Invest. 2011. 121(10):3991-4002. doi: 10.1172/JCI45563McCarthy D.D., Kujawa J., Wilson C. et al. Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy. J Clin Invest. 2011. 121(10):3991-4002. doi: 10.1172/JCI45563Yang C., Mogno I., Contijoch E.J. et al. Fecal IgA Levels Are Determined by Strain-Level Differences in Bacteroides ovatus and Are Modifiable by Gut Microbiota Manipulation. Cell Host Microbe. 2020. 27(3):467-475.e6. doi: 10.1016/j.chom.2020.01.016Yang C., Mogno I., Contijoch E.J. et al. Fecal IgA Levels Are Determined by Strain-Level Differences in Bacteroides ovatus and Are Modifiable by Gut Microbiota Manipulation. Cell Host Microbe. 2020. 27(3):467-475.e6. doi: 10.1016/j.chom.2020.01.016De Angelis M., Montemurno E., Piccolo M. et al. Microbiota and metabolome associated with immunoglobulin A nephropathy (IgAN). PLoS One. 2014. 9(6):e99006. doi: 10.1371/journal.pone.0099006De Angelis M., Montemurno E., Piccolo M. et al. Microbiota and metabolome associated with immunoglobulin A nephropathy (IgAN). PLoS One. 2014. 9(6):e99006. doi: 10.1371/journal.pone.0099006Sallustio F., Curci C., Chaoul N. et al. High levels of gut-homing immunoglobulin A+ B lymphocytes support the pathogenic role of intestinal mucosal hyperresponsiveness in immunoglobulin A nephropathy patients. Nephrol Dial Transplant. 2021. 36(3):452-464. doi: 10.1093/ndt/gfaa264Sallustio F., Curci C., Chaoul N. et al. High levels of gut-homing immunoglobulin A+ B lymphocytes support the pathogenic role of intestinal mucosal hyperresponsiveness in immunoglobulin A nephropathy patients. Nephrol Dial Transplant. 2021. 36(3):452-464. doi: 10.1093/ndt/gfaa264Nyangale E.P., Mottram D.S., Gibson G.R. Gut microbial activity, implications for health and disease: the potential role of metabolite analysis. J Proteome Res. 2012. 11(12):5573-5585. doi: 10.1021/pr300637dNyangale E.P., Mottram D.S., Gibson G.R. Gut microbial activity, implications for health and disease: the potential role of metabolite analysis. J Proteome Res. 2012. 11(12):5573-5585. doi: 10.1021/pr300637dCoppo R., Amore A., Roccatello D. et al. IgA antibodies to dietary antigens and lectin-binding IgA in sera from Italian, Australian, and Japanese IgA nephropathy patients. Am J Kidney Dis. 1991. 17(4):480-487. doi: 10.1016/s0272-6386(12)80644-5Coppo R., Amore A., Roccatello D. et al. IgA antibodies to dietary antigens and lectin-binding IgA in sera from Italian, Australian, and Japanese IgA nephropathy patients. Am J Kidney Dis. 1991. 17(4):480-487. doi: 10.1016/s0272-6386(12)80644-5Yap H.K., Sakai R.S., Woo K.T. et al. Detection of bovine serum albumin in the circulating IgA immune complexes of patients with IgA nephropathy. Clin Immunol Immunopathol. 1987. 43(3):395-402. doi: 10.1016/0090-1229(87)90149-8Yap H.K., Sakai R.S., Woo K.T. et al. Detection of bovine serum albumin in the circulating IgA immune complexes of patients with IgA nephropathy. Clin Immunol Immunopathol. 1987. 43(3):395-402. doi: 10.1016/0090-1229(87)90149-8Sato M., Takayama K., Wakasa M. et al. Estimation of circulating immune complexes following oral challenge with cow's milk in patients with IgA nephropathy. Nephron. 1987. 47(1):43-48. doi: 10.1159/000184455Sato M., Takayama K., Wakasa M. et al. Estimation of circulating immune complexes following oral challenge with cow's milk in patients with IgA nephropathy. Nephron. 1987. 47(1):43-48. doi: 10.1159/000184455Serena G., D’Avino P., Fasano A. Celiac Disease and Non-celiac Wheat Sensitivity: State of Art of Non-dietary Therapies. Front Nutr. 2020. 7:152. doi: 10.3389/fnut.2020.00152Serena G., D’Avino P., Fasano A. Celiac Disease and Non-celiac Wheat Sensitivity: State of Art of Non-dietary Therapies. Front Nutr. 2020. 7:152. doi: 10.3389/fnut.2020.00152Yin J., Yu F.S. Rho kinases regulate corneal epithelial wound healing. Am J Physiol Cell Physiol. 2008. 295:378-387. doi: 10.1152/ajpcell.90624.2007Yin J., Yu F.S. Rho kinases regulate corneal epithelial wound healing. Am J Physiol Cell Physiol. 2008. 295:378-387. doi: 10.1152/ajpcell.90624.2007Tripathi A., Lammers K.M., Goldblum S. et al. Identification of human zonulin, a physiological modulator of tight junctions, as prehaptoglobin-2. Proc Natl Acad Sci U S A. 2009. 106:16799-16804. doi: 10.1073/pnas.0906773106Tripathi A., Lammers K.M., Goldblum S. et al. Identification of human zonulin, a physiological modulator of tight junctions, as prehaptoglobin-2. Proc Natl Acad Sci U S A. 2009. 106:16799-16804. doi: 10.1073/pnas.0906773106Rubio-Tapia A., Murray J.A. Celiac disease. Curr Opin Gastroenterol. 2010. 26:116-122. doi: 10.1097/MOG.0b013e3283365263Rubio-Tapia A., Murray J.A. Celiac disease. Curr Opin Gastroenterol. 2010. 26:116-122. doi: 10.1097/MOG.0b013e3283365263Fasano A. Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev. 2011. 91:151-175. doi: 10.1152/physrev.00003.2008Fasano A. Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol Rev. 2011. 91:151-175. doi: 10.1152/physrev.00003.2008Kim S.M., Mayassi T., Jabri B. Innate immunity: actuating the gears of celiac disease pathogenesis. Best Pract Res Clin Gastroenterol. 2015. 29:425-443. doi: 10.1016/j.bpg.2015.05.001Kim S.M., Mayassi T., Jabri B. Innate immunity: actuating the gears of celiac disease pathogenesis. Best Pract Res Clin Gastroenterol. 2015. 29:425-443. doi: 10.1016/j.bpg.2015.05.001Dieterich W., Ehnis T., Bauer M. et al. Identification of tissue transglutaminase as the autoantigen of celiac disease. Nat Med. 1997. 3:797-801. doi: 10.1038/nm0797-797Dieterich W., Ehnis T., Bauer M. et al. Identification of tissue transglutaminase as the autoantigen of celiac disease. Nat Med. 1997. 3:797-801. doi: 10.1038/nm0797-797Korponay-Szabó I.R., Halttunen T. et al. In vivo targeting of intestinal and extraintestinal transglutaminase 2 by coeliac autoantibodies. Gut. 2004. 53:641-648. doi: 10.1136/gut.2003.024836Korponay-Szabó I.R., Halttunen T. et al. In vivo targeting of intestinal and extraintestinal transglutaminase 2 by coeliac autoantibodies. Gut. 2004. 53:641-648. doi: 10.1136/gut.2003.024836Pasternack A., Collin P., Mustonen J. et al. Glomerular IgA deposits in patients with celiac disease. Clin Nephrol. 1990. 34(2):56-60.Pasternack A., Collin P., Mustonen J. et al. Glomerular IgA deposits in patients with celiac disease. Clin Nephrol. 1990. 34(2):56-60.Woodrow G., Innes A., Boyd S.M. et al. A case of IgA nephropathy with coeliac disease responding to a gluten-free diet. Nephrol Dial Transplant. 1993. 8:1382-1383.Woodrow G., Innes A., Boyd S.M. et al. A case of IgA nephropathy with coeliac disease responding to a gluten-free diet. Nephrol Dial Transplant. 1993. 8:1382-1383.Papista C., Lechner S., Ben Mkaddem S. et al. Gluten exacerbates IgA nephropathy in humanized mice through gliadin-CD89 interaction. Kidney Int. 2015. 88:276-285. doi: 10.1038/ki.2015.94Papista C., Lechner S., Ben Mkaddem S. et al. Gluten exacerbates IgA nephropathy in humanized mice through gliadin-CD89 interaction. Kidney Int. 2015. 88:276-285. doi: 10.1038/ki.2015.94Costa S., Currò G., Pellegrino S. et al. Case report on pathogenetic link between gluten and IgA nephropathy. BMC Gastroenterol. 2018. 18(1):64. doi: 10.1186/s12876-018-0792-0Costa S., Currò G., Pellegrino S. et al. Case report on pathogenetic link between gluten and IgA nephropathy. BMC Gastroenterol. 2018. 18(1):64. doi: 10.1186/s12876-018-0792-0Welаnder A., Sundelin B., Fored M. et al. Increased risk of IgA Nephropathy among individuals with celiac disease. J Clin Gastroenterol. 2013. 47:678-683. doi: 10.1097/MCG.0b013e318284792eWelаnder A., Sundelin B., Fored M. et al. Increased risk of IgA Nephropathy among individuals with celiac disease. J Clin Gastroenterol. 2013. 47:678-683. doi: 10.1097/MCG.0b013e318284792eNurmi R., Pasternack C., Salmi T. et al. J Intern Med. The risk of renal comorbidities in celiac disease patients depends of the phenotype of celiac disease. 2022. 292:279-287. doi: 10.1111/joim.13532Nurmi R., Pasternack C., Salmi T. et al. J Intern Med. The risk of renal comorbidities in celiac disease patients depends of the phenotype of celiac disease. 2022. 292:279-287. doi: 10.1111/joim.13532Collin P., Syrjänen J., Partanen J. et al. Celiac disease and HLA DQ in patients with IgA nephropathy. Am J Gastroenterol. 2002. 97:2572-2576. doi: 10.1111/j.1572-0241.2002.06025.xCollin P., Syrjänen J., Partanen J. et al. Celiac disease and HLA DQ in patients with IgA nephropathy. Am J Gastroenterol. 2002. 97:2572-2576. doi: 10.1111/j.1572-0241.2002.06025.xSlavin S.F. IgA Nephropathy as the Initial Presentation of Celiac Disease in an Adolescent. Pediatrics. 2021. 148(4):e2021051332. doi: 10.1542/peds.2021-051332Slavin S.F. IgA Nephropathy as the Initial Presentation of Celiac Disease in an Adolescent. Pediatrics. 2021. 148(4):e2021051332. doi: 10.1542/peds.2021-051332Habura I., Fiedorowicz K., Wozniak A. et al. IgA nephropathy associated with coeliac disease. Centr Eur J Immunol. 2019. 44 (1):106-108. doi: 10.5114/ceji.2019.84021Habura I., Fiedorowicz K., Wozniak A. et al. IgA nephropathy associated with coeliac disease. Centr Eur J Immunol. 2019. 44 (1):106-108. doi: 10.5114/ceji.2019.84021Welender A., Prutz K.G., Fored M. et al. Increased risk of end-stage renal disease in individuals with celiac disease. Gut. 2012. 61:64-68. doi: 10.1136/gutjnl-2011-300134Welender A., Prutz K.G., Fored M. et al. Increased risk of end-stage renal disease in individuals with celiac disease. Gut. 2012. 61:64-68. doi: 10.1136/gutjnl-2011-300134Coppo R., Amore A., Roccatello D. Dietary antigens and primary immunoglobulin A nephropathy. J Am Soc Nephrol. 1992. 2:173-180. doi: 10.1681/ASN.V210s173Coppo R., Amore A., Roccatello D. Dietary antigens and primary immunoglobulin A nephropathy. J Am Soc Nephrol. 1992. 2:173-180. doi: 10.1681/ASN.V210s173Koivuviita N., Tertti R., Heiro M. et al. A case report: a patient with IgA nephropathy and coeliac disease. Complete clinical remission following gluten-free diet. Nephrol Dial Transplant. 2009. 2:161-163. doi: 10.1093/ndtplus/sfn205Koivuviita N., Tertti R., Heiro M. et al. A case report: a patient with IgA nephropathy and coeliac disease. Complete clinical remission following gluten-free diet. Nephrol Dial Transplant. 2009. 2:161-163. doi: 10.1093/ndtplus/sfn205Salmi T.T., Collin P., Korponay-Szabó I.R. et al. Endomysial antibody-negative coeliac disease: Clinical characteristics and intestinal autoantibody deposits. Gut. 2006. 55:1746-1753. doi: 10.1136/gut.2005.071514Salmi T.T., Collin P., Korponay-Szabó I.R. et al. Endomysial antibody-negative coeliac disease: Clinical characteristics and intestinal autoantibody deposits. Gut. 2006. 55:1746-1753. doi: 10.1136/gut.2005.071514Hadjivassiliou M., Mäki M., Sanders D.S. et al. Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia. Neurology. 2006. 66:373-377. doi: 10.1212/01.wnl.0000196480.55601.3aHadjivassiliou M., Mäki M., Sanders D.S. et al. Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia. Neurology. 2006. 66:373-377. doi: 10.1212/01.wnl.0000196480.55601.3aKoskinen O., Collin P., Korponay-Szabo I. et al. Gluten dependent small bowel mucosal transglutaminase 2-specific IgA deposits in overt and mild enteropathy coeliac disease. J Pediatr Gastroenterol Nutr. 2008. 47:436-442. doi: 10.1097/MPG.0b013e31817b6decKoskinen O., Collin P., Korponay-Szabo I. et al. Gluten dependent small bowel mucosal transglutaminase 2-specific IgA deposits in overt and mild enteropathy coeliac disease. J Pediatr Gastroenterol Nutr. 2008. 47:436-442. doi: 10.1097/MPG.0b013e31817b6decKaukinen K., Peräaho M., Collin P. et al. Small-bowel mucosal transglutaminase 2-specific IgA deposits in coeliac disease without villous atrophy: A prospective and randomized clinical study. Scand J Gastroenterol. 2005. 40:564-572. doi: 10.1080/00365520510023422Kaukinen K., Peräaho M., Collin P. et al. Small-bowel mucosal transglutaminase 2-specific IgA deposits in coeliac disease without villous atrophy: A prospective and randomized clinical study. Scand J Gastroenterol. 2005. 40:564-572. doi: 10.1080/00365520510023422Nurmi R., Korponay-Szabó I., Laurila К. et al. Celiac Disease-Type Tissue Transglutaminase Autoantibody Deposits in Kidney Biopsies of Patients with IgA Nephropathy. Nutrients. 2021. 13(5):1594. doi: 10.3390/nu13051594Nurmi R., Korponay-Szabó I., Laurila К. et al. Celiac Disease-Type Tissue Transglutaminase Autoantibody Deposits in Kidney Biopsies of Patients with IgA Nephropathy. Nutrients. 2021. 13(5):1594. doi: 10.3390/nu13051594

The authors declare that there are no conflicts of interest present.