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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">problendo</journal-id><journal-title-group><journal-title xml:lang="ru">Проблемы Эндокринологии</journal-title><trans-title-group xml:lang="en"><trans-title>Problems of Endocrinology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">0375-9660</issn><issn pub-type="epub">2308-1430</issn><publisher><publisher-name>Endocrinology Research Centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/probl11825</article-id><article-id custom-type="elpub" pub-id-type="custom">problendo-11825</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>Клиническая эндокринология</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Clinical endocrinology</subject></subj-group></article-categories><title-group><article-title>О связи клинических проявлений гломерулонефрита с особенностями тиреоидного статуса больных</article-title><trans-title-group xml:lang="en"><trans-title>About connection of clinical manifestations of glomerulonephritis with features of the thyroid status of patients</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-5899-6352</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Карзакова</surname><given-names>Луиза Михайловна</given-names></name><name name-style="western" xml:lang="en"><surname>Karzakova</surname><given-names>Louise M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор</p></bio><bio xml:lang="en"><p>MD, PhD, Professor</p></bio><email xlink:type="simple">luizak58@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9259-2661</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Автономова</surname><given-names>Ольга Ильинична</given-names></name><name name-style="western" xml:lang="en"><surname>Avtonomova</surname><given-names>Olga I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н.</p></bio><bio xml:lang="en"><p>MD, PhD</p></bio><email xlink:type="simple">olga-aoi@yandex.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-2277-9425</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Кудряшов</surname><given-names>Сергей Игоревич</given-names></name><name name-style="western" xml:lang="en"><surname>Kudryashov</surname><given-names>Sergey I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>ассистент кафедры внутренних болезней</p></bio><bio xml:lang="en"><p>assistant of the Department of internal diseases</p></bio><email xlink:type="simple">medicpro21@mail.ru</email><xref ref-type="aff" rid="aff-3"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-1808-6845</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ухтерова</surname><given-names>Надежда Димитриевна</given-names></name><name name-style="western" xml:lang="en"><surname>Ukhterova</surname><given-names>Nadezhda D.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., доцент</p></bio><bio xml:lang="en"><p>MD, PhD, Associate Professor</p></bio><email xlink:type="simple">55dd@mail.ru</email><xref ref-type="aff" rid="aff-3"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-4155-4849</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Комелягина</surname><given-names>Надежда Анатольевна</given-names></name><name name-style="western" xml:lang="en"><surname>Komelyagina</surname><given-names>Nadezhda А.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., доцент</p></bio><bio xml:lang="en"><p>MD, PhD, Associate Professor</p></bio><email xlink:type="simple">Comelya76@mail.ru</email><xref ref-type="aff" rid="aff-3"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Чувашский государственный университет им. И.Н. Ульянова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Federal State Budgetary Educational Institution of Higher Education “The Chuvash State University named after I.N. Ulyanov”</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Диализный центр «Фрезениус Нефрокеа»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Dialysis Center «Fresenius Nephrokea»</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru"><institution>Чувашский государственный университет им. И.Н. Ульянова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>The Chuvash State University named after I.N. Ulyanov</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2020</year></pub-date><pub-date pub-type="epub"><day>30</day><month>08</month><year>2020</year></pub-date><volume>66</volume><issue>2</issue><fpage>13</fpage><lpage>23</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Карзакова Л.М., Автономова О.И., Кудряшов С.И., Ухтерова Н.Д., Комелягина Н.А., 2020</copyright-statement><copyright-year>2020</copyright-year><copyright-holder xml:lang="ru">Карзакова Л.М., Автономова О.И., Кудряшов С.И., Ухтерова Н.Д., Комелягина Н.А.</copyright-holder><copyright-holder xml:lang="en">Karzakova L.M., Avtonomova O.I., Kudryashov S.I., Ukhterova N.D., Komelyagina N.А.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.probl-endojournals.ru/jour/article/view/11825">https://www.probl-endojournals.ru/jour/article/view/11825</self-uri><abstract><sec><title>ОБОСНОВАНИЕ</title><p>ОБОСНОВАНИЕ. Выделяют четыре клинических варианта гломерулонефрита (ГН) – мочевой (латентный), гипертонический, нефротический и смешанный. Установлено, что особенности клинических проявлений ГН, определяющие его клинический вариант, не зависят от этиологии, патогенеза и морфологической формы заболевания. Обратив внимание на имеющиеся в литературе сведения об ассоциации нефротического синдрома с гипофункцией щитовидной железы, мы предположили, что на формирование клинических вариантов ГН могут влиять особенности тиреоидного статуса больных.</p></sec><sec><title>ЦЕЛЬ</title><p>ЦЕЛЬ. Изучить связь вариантов клинических проявлений ГН с показателями тиреоидного статуса.</p></sec><sec><title>МЕТОДЫ</title><p>МЕТОДЫ. В исследование были включены больные первичным ГН, получавшие стационарное лечение в условиях нефрологического отделения многопрофильной больницы. Больных отбирали в 4 группы в зависимости от клинического варианта ГН (мочевой, нефротический, гипертонический и смешанный варианты). При отборе пациентов добивались сопоставимости групп по возрасту, полу, морфологическим вариантам и продолжительности заболевания. Помимо общепринятых методов исследования, больным проводили: 1) оценку тиреоидного статуса (тиреотропный гормон (ТТГ), свободный тироксин (Т4св.), свободный трийодтиронин (Т3св.), антитела к тиреопероксидазе (анти-ТПО), (Т3св.+Т4св.)/ТТГ, Т4св./Т3св., Т4св./ТТГ); 2) определение уровней интерлейкинов – IL-1β, IL-4 и IL-10 в сыворотке крови; 3) ультразвуковое исследование (УЗИ) щитовидной железы. Полученные данные сравнивали с таковыми у группы здоровых лиц.</p></sec><sec><title>РЕЗУЛЬТАТЫ</title><p>РЕЗУЛЬТАТЫ. В группе пациентов с нефротическим вариантом ГН в 50% случаев обнаруживалось снижение уровня Т4св. на фоне повышения уровня ТТГ, в 26,7% выявлялось умеренное повышение содержания ТТГ при неизмененных концентрациях Т4св. и Т3св. У больных мочевым вариантом ГН тиреоидный статус не отличался от такового у здоровых, а цитокиновый профиль характеризовался одновременным повышением содержания провоспалительного цитокина IL-1β и противовоспалительного цитокина IL-10. У 82% больных гипертоническим вариантом ГН установлено изолированное повышение содержания ТТГ. В группе больных смешанным вариантом ГН преобладали изменения в тиреоидных индексах в сочетании с большой вариабельностью уровня продукции IL-1β.</p></sec><sec><title>ЗАКЛЮЧЕНИЕ</title><p>ЗАКЛЮЧЕНИЕ. Результаты проведенного исследования свидетельствуют о влиянии на формирование различных клинических вариантов ГН функционального состояния гипофизарно-тиреоидной системы, зависящего, в свою очередь, преимущественно от уровня продукции противовоспалительного цитокина IL-10.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>BACKGROUND</title><p>BACKGROUND: There are four clinical variants of glomerulonephritis (GN) - urinary (latent), hypertensive, nephrotic and mixed. It was found that the features of clinical manifestations of GN that determine its clinical variant do not depend on the etiology, pathogenesis and morphological form of the disease. Taking into account the obtained data on the association of nephrotic syndrome with hypofunction of the thyroid gland, we suggested, that the formation of clinical variants of GN may be influenced by the features of the thyroid status of patients.</p></sec><sec><title>AIM</title><p>AIM: Study the relationship of variants of clinical manifestations of GN with indicants of thyroid status.</p></sec><sec><title>MATERIALS AND METHODS</title><p>MATERIALS AND METHODS: The study included patients with primary GN who received in-treatment in the nephrology unit of a general hospital. Patients were selected into 4 groups depending on the clinical variant of GN (urinary, nephrotic, hypertensive and mixed variants). When selecting patients, we achieved comparability of groups by age, gender, morphological variants and duration of the disease. In addition to the generally accepted methods of research, patients were performed: 1) assessment of the thyroid status (thyroid-stimulating hormone (TSH), free thyroxine (free T4), free triiodothyronine (free T3), antibodies to thyroperoxidase (anti-TPO), (free T3+free T4)/TSH, free T4/free T3, free T4/TSH); 2) determination of levels of interleukin - IL-1β, IL-4 and IL-10 in blood serum; 3) ultrasound (US) examination of the thyroid gland. The obtained data were compared with those of healthy people.</p></sec><sec><title>RESULTS</title><p>RESULTS: The group of patients with the nephrotic variant of GN in 50% of cases showed a decrease of the level of free Т4 with the increase of TSH level, 26.7% showed a moderate increase of TSH at unchanged concentrations of free Т4 and free T3. In patients with the urinary variant of GN, the thyroid status did not differ from that in healthy patients, and the cytokine profile was characterized by a simultaneous increase in the content of the proinflammatory cytokine IL-1β and the anti-inflammatory cytokine IL-10. The group of patients with the hypertonic variant of GN in 82% of cases showed an isolated increase in TSH content. In the group of patients with a mixed variant of GN, changes in thyroid indices were predominant, combined with a large variability in the level of IL-1β production.</p></sec><sec><title>CONCLUSIONS</title><p>CONCLUSIONS: The results of the study indicate the influence of the functional state of the pituitary-thyroid system on the formation of different clinical variants of GN, which depends mainly on the level of production of the anti-inflammatory cytokine IL-10.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>тиреоидный статус</kwd><kwd>гломерулонефрит</kwd><kwd>цитокины</kwd><kwd>синдром нетиреоидных заболеваний</kwd></kwd-group><kwd-group xml:lang="en"><kwd>thyroid status</kwd><kwd>glomerulonephritis</kwd><kwd>cytokines</kwd><kwd>euthyroid sick syndrome</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">ФГБОУ ВО «Чувашский государственный университет имени И.Н. Ульянова»</funding-statement><funding-statement xml:lang="en">Federal State Budgetary Educational Institution of Higher Education “The Chuvash State University named after I.N. Ulyanov”</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Нефрология. Клинические рекомендации / Под ред. Е.М. Шилова, А.В. Смирнова, Н.Л. Козловской. — М.: ГЭОТАР-Медиа, 2016. — 816 с. [Nefrologiya. Klinicheskie rekomendacii. Ed. by Shilov E.M., Smirnov A.V., Kozlovskaya N.L. Moscow: GЕOTAR-Media; 2016. 816 р. (In Russ).]</mixed-citation><mixed-citation xml:lang="en">Нефрология. Клинические рекомендации / Под ред. Е.М. Шилова, А.В. Смирнова, Н.Л. Козловской. — М.: ГЭОТАР-Медиа, 2016. — 816 с. [Nefrologiya. Klinicheskie rekomendacii. Ed. by Shilov E.M., Smirnov A.V., Kozlovskaya N.L. Moscow: GЕOTAR-Media; 2016. 816 р. (In Russ).]</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Mario F, Pofi R, Gigante A, et al. Hypothyroidism and nephrotic syndrome: why, when and how to treat. Curr Vasc Pharmacol. 2017;15(5):398–403. doi: 10.2174/1570161115999170207114706F.</mixed-citation><mixed-citation xml:lang="en">Mario F, Pofi R, Gigante A, et al. Hypothyroidism and nephrotic syndrome: why, when and how to treat. Curr Vasc Pharmacol. 2017;15(5):398–403. doi: 10.2174/1570161115999170207114706F.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Marchiori R, Pereira L, Naujorks A, et al. Improvement of blood inflammatory marker levels in patients with hypothyroidism under levothyroxine treatment. BMC Endocr Disord. 2015;15:32. doi: 10.1186/s12902-015-0032-3.</mixed-citation><mixed-citation xml:lang="en">Marchiori R, Pereira L, Naujorks A, et al. Improvement of blood inflammatory marker levels in patients with hypothyroidism under levothyroxine treatment. BMC Endocr Disord. 2015;15:32. doi: 10.1186/s12902-015-0032-3.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Anderson JL, Gruppen EG, van Tienhoven-Wind L, et al. Glomerular filtration rate is associated with free triiodothyronine in euthyroid subjects: Comparison between various equations to estimate renal function and creatinine clearance. Eur J Intern Med. 2018;48:94–99. doi: 10.1016/j.ejim.2017.10.009.</mixed-citation><mixed-citation xml:lang="en">Anderson JL, Gruppen EG, van Tienhoven-Wind L, et al. Glomerular filtration rate is associated with free triiodothyronine in euthyroid subjects: Comparison between various equations to estimate renal function and creatinine clearance. Eur J Intern Med. 2018;48:94–99. doi: 10.1016/j.ejim.2017.10.009.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Dousdampanis P, Trigka K, Vagenakis G, Fourtounas C. The thyroid and the kidney: a complex interplay in health and disease. Int J Artif Organs. 2014;37(1):1–12. doi: 10.5301/ijao.5000300.</mixed-citation><mixed-citation xml:lang="en">Dousdampanis P, Trigka K, Vagenakis G, Fourtounas C. The thyroid and the kidney: a complex interplay in health and disease. Int J Artif Organs. 2014;37(1):1–12. doi: 10.5301/ijao.5000300.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Iglesias P, Bajo MA, Selgas R, Díez JJ. Thyroid dysfunction and kidney disease: an update. Rev Endocr Metab Disord. 2017;18(1):131–144. doi: 10.1007/s11154-016-9395-7.</mixed-citation><mixed-citation xml:lang="en">Iglesias P, Bajo MA, Selgas R, Díez JJ. Thyroid dysfunction and kidney disease: an update. Rev Endocr Metab Disord. 2017;18(1):131–144. doi: 10.1007/s11154-016-9395-7.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Iglesias P, Díez JJ. Thyroid dysfunction and kidney disease. Eur J Endocrinol. 2009;160(4):503–515. doi: 10.1530/eje-08-0837.</mixed-citation><mixed-citation xml:lang="en">Iglesias P, Díez JJ. Thyroid dysfunction and kidney disease. Eur J Endocrinol. 2009;160(4):503–515. doi: 10.1530/eje-08-0837.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">De Vries EM, Fliers E, Boelen A. The molecular basis of the non-thyroidal illness syndrome. J Endocrinol. 2015;225(3):R67–81. doi: 10.1530/JOE-15-0133.</mixed-citation><mixed-citation xml:lang="en">De Vries EM, Fliers E, Boelen A. The molecular basis of the non-thyroidal illness syndrome. J Endocrinol. 2015;225(3):R67–81. doi: 10.1530/JOE-15-0133.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Gutch M, Kumar S, Gupta KK. Prognostic value of thyroid profile in critical care condition. Indian J Endocrinol Metab. 2018;22(3):387–391. doi: 10.4103/ijem.ijem_20_18.</mixed-citation><mixed-citation xml:lang="en">Gutch M, Kumar S, Gupta KK. Prognostic value of thyroid profile in critical care condition. Indian J Endocrinol Metab. 2018;22(3):387–391. doi: 10.4103/ijem.ijem_20_18.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Kanczkowski W, Alexaki VI, Tran N, et al. Hypothalamo-pituitary and immune-dependent adrenal regulation during systemic inflammation. Proc Natl Acad Sci U S A. 2013;110(36):14801–14806. doi: 10.1073/pnas.1313945110.</mixed-citation><mixed-citation xml:lang="en">Kanczkowski W, Alexaki VI, Tran N, et al. Hypothalamo-pituitary and immune-dependent adrenal regulation during systemic inflammation. Proc Natl Acad Sci U S A. 2013;110(36):14801–14806. doi: 10.1073/pnas.1313945110.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Devarapu SK, Anders HJ. Toll-like receptors in lupus nephritis. J Biomed Sci. 2018;25(1):35. doi: 10.1186/s12929-018-0436-2.</mixed-citation><mixed-citation xml:lang="en">Devarapu SK, Anders HJ. Toll-like receptors in lupus nephritis. J Biomed Sci. 2018;25(1):35. doi: 10.1186/s12929-018-0436-2.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Harii N, Lewis CJ, Vasko V, et al. Thyrocytes express a functional toll-like receptor 3: overexpression can be induced by viral infection and reversed by phenylmethimazole and is associated with Hashimoto’s autoimmune thyroiditis. Mol Endocrinol. 2005;19(5):1231–1250. doi: 10.1210/me.2004-0100.</mixed-citation><mixed-citation xml:lang="en">Harii N, Lewis CJ, Vasko V, et al. Thyrocytes express a functional toll-like receptor 3: overexpression can be induced by viral infection and reversed by phenylmethimazole and is associated with Hashimoto’s autoimmune thyroiditis. Mol Endocrinol. 2005;19(5):1231–1250. doi: 10.1210/me.2004-0100.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Yamazaki K, Suzuki K, Yamada E, et al. Suppression of iodide uptake and thyroid hormone synthesis with stimulation of the type I interferon system by double-stranded ribonucleic acid in cultured human thyroid follicles. Endocrinology. 2007;148(7):3226–3235. doi: 10.1210/en.2006-1638.</mixed-citation><mixed-citation xml:lang="en">Yamazaki K, Suzuki K, Yamada E, et al. Suppression of iodide uptake and thyroid hormone synthesis with stimulation of the type I interferon system by double-stranded ribonucleic acid in cultured human thyroid follicles. Endocrinology. 2007;148(7):3226–3235. doi: 10.1210/en.2006-1638.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Zygner W, Gójska-Zygner O, Bąska P, Długosz E. Low T3 syndrome in canine babesiosis associated with increased serum IL-6 concentration and azotaemia. Vet Parasitol. 2015;211(1-2):23–27. doi: 10.1016/j.vetpar.2015.04.023.</mixed-citation><mixed-citation xml:lang="en">Zygner W, Gójska-Zygner O, Bąska P, Długosz E. Low T3 syndrome in canine babesiosis associated with increased serum IL-6 concentration and azotaemia. Vet Parasitol. 2015;211(1-2):23–27. doi: 10.1016/j.vetpar.2015.04.023.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Wheatley T, Edwards O. Mild hypothyroidism and oedema: evidence for increased capillary permeability to protein. Clin Endocrinol (Oxf). 1983;18(6):627–635. doi: 10.1111/j.1365-2265.1983.tb00601.x.</mixed-citation><mixed-citation xml:lang="en">Wheatley T, Edwards O. Mild hypothyroidism and oedema: evidence for increased capillary permeability to protein. Clin Endocrinol (Oxf). 1983;18(6):627–635. doi: 10.1111/j.1365-2265.1983.tb00601.x.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Шилов Е.М., Карзакова Л.М., Автономова О.И., Кудряшов С.И. Иммунные механизмы развития первичных гломерулонефритов // Клиническая медицина. — 2018. — Т.96. — №11. — С. 977–986. [Shilov EM, Karzakova LM, Avtonomova OI, Kudryashov SI. Immune mechanisms of development of primary glomerulonephritis. Klinicheskaia meditsina. 2018;96(11):977–986. (In Russ).]</mixed-citation><mixed-citation xml:lang="en">Шилов Е.М., Карзакова Л.М., Автономова О.И., Кудряшов С.И. Иммунные механизмы развития первичных гломерулонефритов // Клиническая медицина. — 2018. — Т.96. — №11. — С. 977–986. [Shilov EM, Karzakova LM, Avtonomova OI, Kudryashov SI. Immune mechanisms of development of primary glomerulonephritis. Klinicheskaia meditsina. 2018;96(11):977–986. (In Russ).]</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Guo QY, Zhu QJ, Liu YF, et al. Steroids combined with levothyroxine to treat children with idiopathic nephrotic syndrome: a retrospective single-center study. Pediatr Nephrol. 2014;29(6):1033–1038. doi: 10.1007/s00467-013-2727-x.</mixed-citation><mixed-citation xml:lang="en">Guo QY, Zhu QJ, Liu YF, et al. Steroids combined with levothyroxine to treat children with idiopathic nephrotic syndrome: a retrospective single-center study. Pediatr Nephrol. 2014;29(6):1033–1038. doi: 10.1007/s00467-013-2727-x.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Zhu S, Wang Y, Liu H, et al. Thyroxine affects lipopolysaccharide-induced macrophage differentiation and myocardial cell apoptosis via the NF-κB p65 pathway both in vitro and in vivo. Mediators Inflamm. 2019;2019:2098972. doi: 10.1155/2019/2098972.</mixed-citation><mixed-citation xml:lang="en">Zhu S, Wang Y, Liu H, et al. Thyroxine affects lipopolysaccharide-induced macrophage differentiation and myocardial cell apoptosis via the NF-κB p65 pathway both in vitro and in vivo. Mediators Inflamm. 2019;2019:2098972. doi: 10.1155/2019/2098972.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Di MF, Pofi R, Gigante A, et al. Hypothyroidism and nephrotic syndrome: why, when and how to treat. Curr Vasc Pharmacol. 2017;15(5):398–403. doi: 10.2174/1570161115999170207114706.</mixed-citation><mixed-citation xml:lang="en">Di MF, Pofi R, Gigante A, et al. Hypothyroidism and nephrotic syndrome: why, when and how to treat. Curr Vasc Pharmacol. 2017;15(5):398–403. doi: 10.2174/1570161115999170207114706.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Jain D, Aggarwal HK, Pavan Kumar YM, Jain P. Evaluation of thyroid dysfunction in patients with nephrotic syndrome. Med Pharm Rep. 2019;92(2):139–144. doi: 10.15386/mpr-1091.</mixed-citation><mixed-citation xml:lang="en">Jain D, Aggarwal HK, Pavan Kumar YM, Jain P. Evaluation of thyroid dysfunction in patients with nephrotic syndrome. Med Pharm Rep. 2019;92(2):139–144. doi: 10.15386/mpr-1091.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Chang YC, Chang CH, Yeh YC, et al. Subclinical and overt hypothyroidism is associated with reduced glomerular filtration rate and proteinuria: a large cross-sectional population study. Sci Rep. 2018;8(1):2031. doi: 10.1038/s41598-018-19693-4.</mixed-citation><mixed-citation xml:lang="en">Chang YC, Chang CH, Yeh YC, et al. Subclinical and overt hypothyroidism is associated with reduced glomerular filtration rate and proteinuria: a large cross-sectional population study. Sci Rep. 2018;8(1):2031. doi: 10.1038/s41598-018-19693-4.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Huang Y, Feng L, Li X, et al. Clinical observation and analysis of thyroid hormone levels in patients with idiopathic membranous nephropathy. Medicine (Baltimore). 2020;99(7):e19106. doi: 10.1097/MD.0000000000019106.</mixed-citation><mixed-citation xml:lang="en">Huang Y, Feng L, Li X, et al. Clinical observation and analysis of thyroid hormone levels in patients with idiopathic membranous nephropathy. Medicine (Baltimore). 2020;99(7):e19106. doi: 10.1097/MD.0000000000019106.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Jung SH, Lee JE, Chung WY. Changes in the thyroid hormone profiles in children with nephrotic syndrome. Korean J Pediatr. 2019;62(3):85–89. doi: 10.3345/kjp.2018.06891.</mixed-citation><mixed-citation xml:lang="en">Jung SH, Lee JE, Chung WY. Changes in the thyroid hormone profiles in children with nephrotic syndrome. Korean J Pediatr. 2019;62(3):85–89. doi: 10.3345/kjp.2018.06891.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Yoshida K, Sakurada T, Kaise K, et al. Measurement of thyroid stimulating hormone (TSH) in human urine. Endocrinol Jpn. 1988;35(5):733–739. doi: 10.1507/endocrj1954.35.733.</mixed-citation><mixed-citation xml:lang="en">Yoshida K, Sakurada T, Kaise K, et al. Measurement of thyroid stimulating hormone (TSH) in human urine. Endocrinol Jpn. 1988;35(5):733–739. doi: 10.1507/endocrj1954.35.733.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Яглова Н.В. Синдром нетиреоидных заболеваний при остром бактериальном эндотоксикозе: патогенетические механизмы и методы коррекции // Вестник РАМН. — 2013. — №3. — С. 24–32. [Yaglova NV. Non-thyroid disease syndrome in acute bacterial endotoxemia: pathogenetic mechanisms and methods of correction. Annals of the Russian Academy of Medical Sciences. 2013;(3):24–32. (In Russ).]</mixed-citation><mixed-citation xml:lang="en">Яглова Н.В. Синдром нетиреоидных заболеваний при остром бактериальном эндотоксикозе: патогенетические механизмы и методы коррекции // Вестник РАМН. — 2013. — №3. — С. 24–32. [Yaglova NV. Non-thyroid disease syndrome in acute bacterial endotoxemia: pathogenetic mechanisms and methods of correction. Annals of the Russian Academy of Medical Sciences. 2013;(3):24–32. (In Russ).]</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Morris M, Bostom A, Jacques P, et al. Hyperhomocysteinemia and hypercholesterolemia associated with hypothyroidism in the third US National Health and Nutrition Examination Survey. Atherosclerosis. 2001;155(1):195–200. doi: 0.1016/s0021-9150(00)00537-2.</mixed-citation><mixed-citation xml:lang="en">Morris M, Bostom A, Jacques P, et al. Hyperhomocysteinemia and hypercholesterolemia associated with hypothyroidism in the third US National Health and Nutrition Examination Survey. Atherosclerosis. 2001;155(1):195–200. doi: 0.1016/s0021-9150(00)00537-2.</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Weber GJ, Pushpakumar S, Tyagi SC, Sen U. Homocysteine and hydrogen sulfide in epigenetic, metabolic and microbiota related renovascular hypertension. Pharmacol Res. 2016;113(Pt A):300–312. doi: 10.1016/j.phrs.2016.09.002.</mixed-citation><mixed-citation xml:lang="en">Weber GJ, Pushpakumar S, Tyagi SC, Sen U. Homocysteine and hydrogen sulfide in epigenetic, metabolic and microbiota related renovascular hypertension. Pharmacol Res. 2016;113(Pt A):300–312. doi: 10.1016/j.phrs.2016.09.002.</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Guven-Maiorov E, Keskin O, Gursoy A, et al. The architecture of the TIR domain signalosome in the toll-like Receptor-4 signaling pathway. Sci Rep. 2015;5:13128. doi: 10.1038/srep13128.</mixed-citation><mixed-citation xml:lang="en">Guven-Maiorov E, Keskin O, Gursoy A, et al. The architecture of the TIR domain signalosome in the toll-like Receptor-4 signaling pathway. Sci Rep. 2015;5:13128. doi: 10.1038/srep13128.</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Dvornikova KA, Bystrova EY, Platonova ON, Churilov LP. Polymorphism of toll-like receptor genes and autoimmune endocrine diseases. Autoimmun Rev. 2020;19(4):102496. doi: 10.1016/j.autrev.2020.102496.</mixed-citation><mixed-citation xml:lang="en">Dvornikova KA, Bystrova EY, Platonova ON, Churilov LP. Polymorphism of toll-like receptor genes and autoimmune endocrine diseases. Autoimmun Rev. 2020;19(4):102496. doi: 10.1016/j.autrev.2020.102496.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
