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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">detinf</journal-id><journal-title-group><journal-title xml:lang="ru">ДЕТСКИЕ ИНФЕКЦИИ</journal-title><trans-title-group xml:lang="en"><trans-title>CHILDREN INFECTIONS</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2072-8107</issn><issn pub-type="epub">2618-8139</issn><publisher><publisher-name>Association of Pediatricians and Infection Disease doctors</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.22627/2072-8107-2025-24-1-51-55</article-id><article-id custom-type="elpub" pub-id-type="custom">detinf-1035</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>ЛЕКЦИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>LECTURE</subject></subj-group></article-categories><title-group><article-title>Генетические полиморфизмы и острое повреждение почек</article-title><trans-title-group xml:lang="en"><trans-title>Genetic polymorphisms and acute kidney injury</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-0895-6707</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Мазанкова</surname><given-names>Л. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Mazankova</surname><given-names>L. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Мазанкова Людмила Николаевна, д.м.н., профессор, ФГБОУ ДПО РМАНПО, гл. внештатный специалист по инфекционным болезням у детей</p><p>Москва</p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">mazankova@list.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/0000-0002-3240-8655</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Савинкова</surname><given-names>П. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>Savinkova</surname><given-names>P. Y.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Савинкова Полина Юрьевна, врач-педиатр, аспирант кафедры детских инфекционных болезней, РМАНПО</p><p>Москва</p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">polinkaluzan@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">ФГБОУ ДПО Российская медицинская академия непрерывного профессионального образования МЗ РФ<country>Россия</country></aff><aff xml:lang="en">FGBOU DPO RMAPO of the Ministry of Health of Russia<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>24</day><month>03</month><year>2025</year></pub-date><volume>24</volume><issue>1</issue><fpage>51</fpage><lpage>55</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Мазанкова Л.Н., Савинкова П.Ю., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Мазанкова Л.Н., Савинкова П.Ю.</copyright-holder><copyright-holder xml:lang="en">Mazankova L.N., Savinkova P.Y.</copyright-holder><license 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://detinf.elpub.ru/jour/article/view/1035">https://detinf.elpub.ru/jour/article/view/1035</self-uri><abstract><p>Острое повреждение почек (ОПП) является одним из наиболее серьезных осложнений инфекционных заболеваний, с частотой возникновения от 5% до 30—50% среди госпитализированных пациентов. Несмотря на достижения в лечении ОПП, включая заместительную почечную терапию, заболеваемость и смертность продолжают расти. Наблюдается значительная вариабельность клинических проявлений ОПП у пациентов с идентичной патологией, что подчеркивает необходимость изучения дополнительных факторов, влияющих на тяжесть и исходы заболевания. Важную роль в этом процессе может играть генетическая изменчивость, включая полиморфизм генов, который определяет индивидуальные особенности регуляторных механизмов при повреждении почек. Данная статья направлена на анализ существующих данных о влиянии генетических факторов на развитие и исходы ОПП, а также изучение полиморфизмов генов, которые могут служить диагностическими критериями для раннего выявления и риска развития ОПП. Акцентируется внимание на генах, связанных с воспалительным ответом, таких как TNF-á, IL-1â, IL-6, IL-8, IFN-ã, TGF-â и IL-10, и их потенциальной роли в предрасположенности к ОПП и течению заболевания. Описывается также влияние генетических вариаций вазомоторных регуляторных белков, таких как ангиотензинпревращающий фермент (АПФ) и эндотелиальная синтаза оксида азота (eNOS), на развитие ОПП. Проанализирована связь между полиморфизмами в генах BCL2 и SERPINA с ОПП, а также между полиморфизмами генов SERPINA4 и SERPINA5 и развитием ОПП у пациентов с COVID-19. Несмотря на множество исследований и выявленные ассоциации, данные о генетических факторах риска остаются ограниченными и противоречивыми, что подчеркивает необходимость дальнейших исследований. Выявление новых генетических маркеров поможет улучшить диагностику и обеспечить индивидуализированный подход к профилактике и лечению ОПП, особенно у детей с высокой предрасположенностью к данному состоянию.</p></abstract><trans-abstract xml:lang="en"><p>Acute kidney injury (AKI) is one of the most serious complications of infectious diseases, occurring in 5% to 30—50% of hospitalized patients. Despite advances in the treatment of AKI, including renal replacement therapy, morbidity and mortality rates continue to rise. There is significant variability in the clinical manifestations of AKI among patients with identical pathology, highlighting the need to study additional factors that influence the severity and outcomes of the disease. Genetic variability, including gene polymorphisms that determine individual characteristics of regulatory mechanisms in kidney damage, may play an important role in this process. This article aims to analyze existing data on the impact of genetic factors on the development and outcomes of AKI, as well as gene polymorphisms that may serve as diagnostic criteria for early detection and risk of AKI. The focus is on genes associated with the inflammatory response, such as TNF-á, IL-1â, IL-6, IL-8, IFN-ã, TGF-â, and IL-10, and their potential role in predisposition to AKI and disease progression. The influence of genetic variations in vasomotor regulatory proteins, such as angiotensin-converting enzyme (ACE) and endothelial nitric oxide synthase (eNOS), on the development of AKI is also discussed. The relationship between polymorphisms in the BCL2 and SERPINA genes and AKI, as well as between polymorphisms in the SERPINA4 and SERPINA5 genes and the development of AKI in COVID-19 patients, is analyzed. Despite numerous studies and identified associations, data on genetic risk factors remain limited and contradictory, underscoring the need for further research. The identification of new genetic markers will help improve diagnosis and provide a personalized approach to the prevention and treatment of AKI, especially in children with a high predisposition to this condition.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>острое повреждение почек</kwd><kwd>SARS-Cov-2</kwd><kwd>COVID-19</kwd><kwd>генетический полиморфизм</kwd><kwd>цитокины</kwd><kwd>фактор некроза опухоли альфа (TNF-α)</kwd><kwd>интерлейкин-1 бета (IL-1β)</kwd><kwd>интерлейкин-6 (IL6)</kwd><kwd>интерлейкин-8 (CXCL8)</kwd><kwd>интерферон гамма (IFNγ)</kwd><kwd>трансформирующий фактор роста бета (TGF-β)</kwd><kwd>интерлейкин-10 (IL10)</kwd><kwd>ангиотензинпревращающий фермент (АПФ)</kwd><kwd>эндотелиальная синтаза оксида азота (eNOS)</kwd><kwd>BCL2</kwd><kwd>SERPINA</kwd><kwd>биомаркеры</kwd><kwd>NGAL — липокалин-2</kwd><kwd>ассоциированный с нейтрофильной желатиназой</kwd><kwd>KIM-1 — молекула повреждения почек</kwd><kwd>L-FABP — белок</kwd><kwd>связывающий жирные кислоты печеночного типа</kwd><kwd>IL-18 — интерлейкин-18</kwd><kwd>Цистатин С</kwd><kwd>нефрин</kwd></kwd-group><kwd-group xml:lang="en"><kwd>Acute kidney injury</kwd><kwd>SARS-Cov-2</kwd><kwd>COVID-19</kwd><kwd>genetic polymorphism</kwd><kwd>cytokines</kwd><kwd>tumor necrosis factor alpha (TNF-α)</kwd><kwd>interleukin-1 beta (IL-1β)</kwd><kwd>interleukin-6 (IL-6)</kwd><kwd>interleukin-8 (CXCL8)</kwd><kwd>interferon gamma (IFNγ)</kwd><kwd>transforming growth factor beta (TGF-β)</kwd><kwd>interleukin-10 (IL10)</kwd><kwd>angiotensin-converting enzyme (ACE)</kwd><kwd>endothelial nitric oxide synthase (eNOS)</kwd><kwd>BCL2</kwd><kwd>SERPINA</kwd><kwd>biomarkers</kwd><kwd>NGAL — neutrophil gelatinase-associated lipocalin-2</kwd><kwd>KIM-1 — kidney injury molecule</kwd><kwd>L-FABP — liver-type fatty acid binding protein</kwd><kwd>IL-18 — interleukin-18</kwd><kwd>Cystatin C</kwd><kwd>nephrin</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">Xue JL, Daniels F, Star RA, Kimmel PL, Eggers PW, Molitoris BA, Himmelfarb J, Collins AJ. 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