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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">nid</journal-id><journal-title-group><journal-title xml:lang="ru">Нефрология и диализ</journal-title><trans-title-group xml:lang="en"><trans-title>Nephrology and Dialysis</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1680-4422</issn><issn pub-type="epub">2618-9801</issn><publisher><publisher-name>Российское диализное общество</publisher-name></publisher></journal-meta><article-meta><article-id custom-type="elpub" pub-id-type="custom">nid-3190</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 И ЛЕКЦИИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS AND LECTURES</subject></subj-group></article-categories><title-group><article-title>Роль витамина Д и кальция в иммунопатологии почек и артериальной гипертензии</article-title><trans-title-group xml:lang="en"><trans-title>The role of vitamin D and calcium in kidney immunopathology and arterial hypertension</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Руснак</surname><given-names>Ф. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Rusnak</surname><given-names>F. I.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff xml:lang="ru" id="aff-1"><institution>Детская клиническая больница № 38, г. Москва</institution><country>Russian Federation</country></aff><pub-date pub-type="collection"><year>2002</year></pub-date><pub-date pub-type="epub"><day>28</day><month>06</month><year>2025</year></pub-date><volume>4</volume><issue>2</issue><fpage>86</fpage><lpage>92</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Руснак Ф.И., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Руснак Ф.И.</copyright-holder><copyright-holder xml:lang="en">Rusnak F.I.</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://journal.nephro.ru/jour/article/view/3190">https://journal.nephro.ru/jour/article/view/3190</self-uri><abstract><p>Необходимым условием выполнения витамином D своих функций является его последовательное превращение в печени и почках с образованием 25-гидрокси-витамина D3 (25D) и 1,25D или 24,25 дигидроксивитамина D3 (24,25D). 25D является транспортной формой витамина D, а 1,25D - его гормональной формой, механизм действия которой аналогичен таковому других стероидных гормонов. Данные о физиологической роли 24,25D противоречивы, но он обладает также некоторыми свойствами гормона. Витамин D поступает в организм с пищей, а также образуется в коже из 7-дегидрохолестерина. Витамин D переносится в печень, где осуществляется включение гидроксильной группы в С25 положении. Образующийся 25D является основной циркулирующей формой витамина D. Кроме того, этот метаболит в небольших количествах образуется в кишечнике, почках и легких. Механизм регуляции образования 25D нe вполне ясен. Известны его сезонные и географические колебания, коррелирующие с интенсивностью инсоляции, возрастание его концентрации при дополнительном введении витамина D, что может свидетельствовать о нежесткой регуляции по механизму обратной связи. Так, при обследовании 15 детей с ХПН в результате тубулоинтерстициальных болезней почек (креатинин крови 2,3 + 1,3 мг%, клиренс креатинина 36 + 20 мл/мин), уровень 25D в крови в летние месяцы (июль-сентябрь) был в пределах 34 нг/мл (у здоровых - 30 нг/мл), в зимние (октябрь-май) - 20 нг/мл (у здоровых - 16 нг/мл), т. е. в зимние месяцы уровень 25D снижается примерно на 50%, как у здоровых детей, так и у пациентов с ХПН [<xref ref-type="bibr" rid="cit55">55</xref>]. 1,25D снижает активность 25-гидроксилазы в печени и ускоряет деградацию 25D, что приводит к снижению его концентрации в крови. Образовавшийся 25D связывается в основном с альбуминами (витамин-D-связывающий белок - ВDБ) или подвергается энтерогепатической рециркуляции. Период полужизни 25D в крови - 20-30 суток. 25D используется как показатель обеспеченности организма витамином D.</p></abstract><kwd-group xml:lang="ru"><kwd>кальцитриол (1</kwd><kwd>25D)</kwd><kwd>кальций</kwd><kwd>иммунитет</kwd><kwd>гломерулонефрит</kwd><kwd>ХПН</kwd><kwd>ПТГ</kwd><kwd>артериальная гипертензия</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">Бауман В.К. Биохимия и физиология витамина Д. Рига, 1989: 480 с.</mixed-citation><mixed-citation xml:lang="en">Бауман В.К. Биохимия и физиология витамина Д. Рига, 1989: 480 с.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Болдырев А.А., Мельгунов В.И. Транспортные АТФ-азы. Итоги науки и техники ВИНИТИ. Сер. Биофизика. М., 1985: 241 с.</mixed-citation><mixed-citation xml:lang="en">Болдырев А.А., Мельгунов В.И. Транспортные АТФ-азы. 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