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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">nogr</journal-id><journal-title-group><journal-title xml:lang="ru">Экспериментальная и клиническая гастроэнтерология</journal-title><trans-title-group xml:lang="en"><trans-title>Experimental and Clinical Gastroenterology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1682-8658</issn><publisher><publisher-name>«Global Media Technologies»</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.31146/1682-8658-ecg-235-3-104-118</article-id><article-id custom-type="elpub" pub-id-type="custom">nogr-3138</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>МЕТАБОЛИЧЕСКИЙ СИНДРОМ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>METABOLIC SYNDROME</subject></subj-group></article-categories><title-group><article-title>Хроническая болезнь почек приводит к истощению скелетной мускулатуры</article-title><trans-title-group xml:lang="en"><trans-title>Chronic kidney disease leads to skeletal muscle wasting</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-0027-1786</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Булгакова</surname><given-names>С. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Bulgakova</surname><given-names>S. V.</given-names></name></name-alternatives><email xlink:type="simple">osteoporosis63@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/0000-0003-4114-5233</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Курмаев</surname><given-names>Д. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Kurmaev</surname><given-names>D. P.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.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/0000-0003-0097-7252</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Тренева</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Treneva</surname><given-names>E. V.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное образовательное учреждение высшего образования «Самарский государственный медицинский университет» Министерства здравоохранения Российской Федерации</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Samara State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>29</day><month>10</month><year>2025</year></pub-date><volume>0</volume><issue>3</issue><fpage>104</fpage><lpage>118</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Булгакова С.В., Курмаев Д.П., Тренева Е.В., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Булгакова С.В., Курмаев Д.П., Тренева Е.В.</copyright-holder><copyright-holder xml:lang="en">Bulgakova S.V., Kurmaev D.P., Treneva E.V.</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.nogr.org/jour/article/view/3138">https://www.nogr.org/jour/article/view/3138</self-uri><abstract><p>Саркопения - заболевание, которое характеризуется прогрессивным снижением силы, массы и функции скелетной мускулатуры. Причинами развития саркопении является старение, гиподинамия, нарушение нутритивного статуса и сопутствующие заболевания. Хроническая болезнь почек (ХБП) может явиться важным фактором риска развития саркопении, так как оказывает негативные эффекты на системном уровне. Альбуминурия и протеинурия приводят к отрицательному азотистому балансу в организме, когда потеря белка превышает его синтез. Накопление уремических токсинов на фоне ХБП способствуют системному воспалению и катаболизму мышечной ткани. Присоединяющийся на поздних стадиях ХБП кардиоренальный синдром способствует усугублению системных нарушений и присоединению сердечной недостаточности. Все вышеперечисленные механизмы патогенеза приводят к нарушению синтеза и усилению деградации белков мышечной ткани. Поэтому лечение саркопении на фоне ХБП должно быть комплексным, с учетом степени нарушения функции почек.</p></abstract><trans-abstract xml:lang="en"><p>Sarcopenia is a disease characterized by a strong progressive decrease in the mass and functions of skeletal muscles. The causes of sarcopenia are aging, physical inactivity, impaired nutritional effects and concomitant diseases. Chronic kidney disease (CKD) can be a prerequisite for the development of sarcopenia, and also have a negative effect on the systemic level. Albuminuria and proteinuria lead to a negative nitrogen balance as a result, when the loss of protein leads to its synthesis. The accumulation of uremic toxins against the background of CKD contribute to systemic inflammation and catabolism of muscle tissue. Joining in the late stages of the cardiorenal syndrome of CKD, aggravation of systemic disorders and limitation of heart failure are ensured. All of the above mechanisms of pathogenesis lead to impaired synthesis and increased degradation of cellular tissue proteins. Therefore, the treatment of sarcopenia against the background of CKD should be comprehensive, taking into account the degree of renal dysfunction.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>хроническая болезнь почек</kwd><kwd>саркопения</kwd><kwd>альбуминурия</kwd><kwd>протеинурия</kwd><kwd>катаболический синдром</kwd><kwd>незаменимые аминокислоты</kwd><kwd>заместительная почечная терапия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>chronic kidney disease</kwd><kwd>sarcopenia</kwd><kwd>albuminuria</kwd><kwd>proteinuria</kwd><kwd>catabolic syndrome</kwd><kwd>essential amino acids</kwd><kwd>renal replacement therapy</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Andreev D.A., Kamynina N.N. 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