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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">diaendo</journal-id><journal-title-group><journal-title xml:lang="ru">Сахарный диабет</journal-title><trans-title-group xml:lang="en"><trans-title>Diabetes mellitus</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2072-0351</issn><issn pub-type="epub">2072-0378</issn><publisher><publisher-name>Endocrinology research centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/DM12944</article-id><article-id custom-type="elpub" pub-id-type="custom">diaendo-12944</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>Обзоры</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Хроническая болезнь почек у пациентов с сахарным диабетом 2 типа: новые мишени лекарственного воздействия</article-title><trans-title-group xml:lang="en"><trans-title>Chronic kidney disease in patients with type 2 diabetes: new targets of medicine action</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3838-8285</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Трубицына</surname><given-names>Н. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Trubitsyna</surname><given-names>N. P.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Трубицына Наталья Петровна - кандидат медицинских наук, ведущий научный сотрудник.</p><p>117036, Москва, ул. Дм. Ульянова, д. 11</p></bio><bio xml:lang="en"><p>Natalia P. Trubitsyna - MD, PhD, leading research associate.</p><p>11, Dm. Ul’yanova st., Moscow, 117036</p></bio><email xlink:type="simple">trubicina@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/0000-0001-9235-5594</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Зайцева</surname><given-names>Н. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Zaitseva</surname><given-names>N. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Зайцева Наталья Владиславовна - кандидат медицинских наук, ведущий научный сотрудник; eLibrary SPIN: 8894-8815.</p><p>Москва</p></bio><bio xml:lang="en"><p>Natalia V. Zaitseva - MD, PhD, leading research associate; eLibrary SPIN: 8894-8815.</p><p>Moscow</p></bio><email xlink:type="simple">nata.zaec@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-0296-4933</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Северина</surname><given-names>А. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Severinа</surname><given-names>A. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Северина Анастасия Сергеевна - кандидат медицинских наук, ведущий научный сотрудник; eLibrary SPIN: 3182-9510.</p><p>Москва</p></bio><bio xml:lang="en"><p>Anastasia S. Severina - MD, PhD, leading research associate; eLibrary SPIN: 3182-9510.</p><p>Moscow</p></bio><email xlink:type="simple">ansev1@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/0000-0002-3433-0142</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шамхалова</surname><given-names>М. Ш.</given-names></name><name name-style="western" xml:lang="en"><surname>Shamkhalova</surname><given-names>M. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Шамхалова Минара Шамхаловна - доктор медицинских наук; eLibrary SPIN: 4942-5481.</p><p>Москва</p></bio><bio xml:lang="en"><p>Minara S. Shamhalova - MD, PhD; eLibrary SPIN: 4942-5481.</p><p>Moscow</p></bio><email xlink:type="simple">shamkhalova@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Национальный медицинский исследовательский центр эндокринологии</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Endocrinology Research Centre</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2022</year></pub-date><pub-date pub-type="epub"><day>30</day><month>11</month><year>2022</year></pub-date><volume>25</volume><issue>5</issue><fpage>492</fpage><lpage>498</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Трубицына Н.П., Зайцева Н.В., Северина А.С., Шамхалова М.Ш., 2022</copyright-statement><copyright-year>2022</copyright-year><copyright-holder xml:lang="ru">Трубицына Н.П., Зайцева Н.В., Северина А.С., Шамхалова М.Ш.</copyright-holder><copyright-holder xml:lang="en">Trubitsyna N.P., Zaitseva N.V., Severinа A.S., Shamkhalova M.S.</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.dia-endojournals.ru/jour/article/view/12944">https://www.dia-endojournals.ru/jour/article/view/12944</self-uri><abstract><p>Сахарный диабет 2 типа (СД2) — социально значимое заболевание, которое по темпу роста распространенности приобретает характер неинфекционной эпидемии. Хроническая болезнь почек (ХБП) является одним из наиболее частых осложнений СД2. Признаки повреждения почек и/или снижение скорости клубочковой фильтрации (СКФ) выявляют у 40–50% пациентов с СД2. Считается, что в основе развития и прогрессирования ХБП на фоне СД2 лежат три группы факторов: метаболические, гемодинамические, а также факторы воспаления и фиброза. Препараты, применяемые в настоящее время у пациентов с ХБП и СД2, в первую очередь направлены на коррекцию гемодинамических и метаболических нарушений, а на процессы воспаления и фиброза воздействуют лишь косвенно. Гиперактивация минералокортикоидных рецепторов (МКР) рассматривается в качестве одного из основных пусковых механизмов повреждения органов-мишеней у пациентов с СД2 за счет потенцирования воспаления и фиброза. Разработка и изучение препаратов из нового класса селективных нестероидных антагонистов МКР (АМКР) направлены на получение доказательств положительных эффектов от блокирования данного патофизиологического пути развития ХБП и преодоление недостатков, характерных для стероидных АМКР. Таким образом, патологическая гипер­активация МКР с развитием воспаления и фиброза у пациентов с ХБП на фоне СД2 представляется перспективной терапевтической мишенью для реализации таргетной кардионефропротективной терапии новыми лекарственными препаратами.</p></abstract><trans-abstract xml:lang="en"><p>Diabetes mellitus type 2 (DM2) is socially important disease, becoming non-infectious epidemic due to increasing prevalence. Chronic kidney disease (CKD) is one of the most common diabetic complications. Kidney injury signs and/or estimated glomerular filtration rate (eGFR) decrease are seen in 40-50% of patients with DM2. Three groups of factors are considered to be the basis of CKD development and progression in DM2: metabolic, hemodynamic, inflammation and fibrosis. Existing drugs that are used in patients with CKD and DM2 first of all target hemodynamic and metabolic disturbances, but their action against inflammation and fibrosis is indirect. Hyperactivation of mineralocorticoid receptors (MR) is considered as one of the main trigger factors of end-organ damage in patients with DM2 due to inflammation and fibrosis. Development of selective nonsteroidal MR antagonists (MRA) as a new class of medications is directed to demonstrate positive effects from blocking this pathophysiological pathway of CKD development and overcome the steroidal MRAs’ shortcomings. Hence pathophysiological hyperactivation of MR with subsequent inflammation and fibrosis in patients with CKD in DM2 is considered a promising therapeutic target for the new drugs with cardionephroprotective effect.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>сахарный диабет 2 типа</kwd><kwd>хроническая болезнь почек</kwd><kwd>воспаление</kwd><kwd>фиброз</kwd><kwd>нестероидные селективные антагонисты минералокортикоидных рецепторов</kwd></kwd-group><kwd-group xml:lang="en"><kwd>diabetes mellitus type 2</kwd><kwd>сhronic kidney disease</kwd><kwd>inflammation</kwd><kwd>fibrosis</kwd><kwd>non-steroid selective mineralocorticoid receptors antagonists</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Публикация подготовлена при поддержке АО «Байер». 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