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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">cardiotomsk</journal-id><journal-title-group><journal-title xml:lang="ru">Сибирский журнал клинической и экспериментальной медицины</journal-title><trans-title-group xml:lang="en"><trans-title>Siberian Journal of Clinical and Experimental Medicine</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2713-2927</issn><issn pub-type="epub">2713-265X</issn><publisher><publisher-name>TSU publishing</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.29001/2073-8552-2020-35-2-81-88</article-id><article-id custom-type="elpub" pub-id-type="custom">cardiotomsk-979</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>КЛИНИЧЕСКИЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CLINICAL STUDIES</subject></subj-group></article-categories><title-group><article-title>Особенности формирования хронической сердечной недостаточности у больных персистирующей формой фибрилляции предсердий в зависимости от фенотипа почечной дисфункции</article-title><trans-title-group xml:lang="en"><trans-title>Peculiarities of chronic heart failure formation in patients with persistent atrial fi brillation depending on the renal dysfunction phenotype</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-3694-3647</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Полянская</surname><given-names>Е. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Polyanskaya</surname><given-names>E. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>канд. мед. наук, доцент кафедры пропедевтики внутренних болезней № 2,</p><p>614990, Пермский край, Пермь, ул. Петропавловская, 26</p></bio><bio xml:lang="en"><p>Cand. Sci. (Med.), Associate Professor, Department of Propedeutics of Internal Diseases No. 2,</p><p>26, Petropavlovskaya str., Perm, 614990</p></bio><email xlink:type="simple">eapolyanskaya@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/0000-0001-7003-5186</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Козиолова</surname><given-names>Н. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Koziolova</surname><given-names>N. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д-р мед наук, профессор, заведующий кафедрой пропедевтики внутренних болезней № 2,</p><p>614990, Пермский край, Пермь, ул. Петропавловская, 26</p></bio><bio xml:lang="en"><p>Dr. Sci. (Med.), Professor, Head of the Department of Propedeutics of Internal Diseases No. 2,</p><p>26, Petropavlovskaya str., Perm, 614990</p></bio><email xlink:type="simple">nakoziolova@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Пермский государственный медицинский университет имени академика Е.А. Вагнера Министерства здравоохранения&#13;
Российской Федерации</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Perm State Medical University named after Academician E.A. Wagner</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2020</year></pub-date><pub-date pub-type="epub"><day>06</day><month>07</month><year>2020</year></pub-date><volume>35</volume><issue>2</issue><fpage>81</fpage><lpage>88</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Полянская Е.А., Козиолова Н.А., 2020</copyright-statement><copyright-year>2020</copyright-year><copyright-holder xml:lang="ru">Полянская Е.А., Козиолова Н.А.</copyright-holder><copyright-holder xml:lang="en">Polyanskaya E.A., Koziolova N.A.</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.sibjcem.ru/jour/article/view/979">https://www.sibjcem.ru/jour/article/view/979</self-uri><abstract><sec><title>Цель</title><p>Цель: изучить особенности формирования хронической сердечной недостаточности (ХСН) у больных персистирующей формой фибрилляции предсердий (ФП) в зависимости от фенотипа ренальной дисфункции.</p></sec><sec><title>Материал и методы</title><p>Материал и методы. В исследование включены 60 пациентов с персистирующей формой ФП и ХСН. Для диагностики ХСН проводили эхокардиографическое (ЭхоКГ) исследование, определяли концентрацию NT-рrоBNP и sST2 в сыворотке крови. Фильтрационную функцию почек оценивали по скорости клубочковой фильтрации СКФ, рассчитанной на основе креатинина и цистатина С; нарушения функции канальцев – по концентрации NGAL (Neutrophil Gelatinase-Associated Lipocalin) в плазме. Были выделены три фенотипа почечного повреждения. В 1-ю группу вошли 14 (23,3%) человек с изолированной канальцевой дисфункцией, оцененной по NGAL, во 2-ю группу – 14 (23,3%) пациентов с изолированной клубочковой дисфункцией, оцененной по СКФ (CKD-EPIcys), в 3-ю группу – 32 (53,3%) больных с сочетанием канальцевой и клубочковой дисфункции.</p></sec><sec><title>Результаты</title><p>Результаты. У 36,7% больных во 2-й и 3-й группах значение СКФ (CKD-EPIcre) было ниже 60 мл/мин/1,73 м2 . Концентрация цистатина С статистически значимо отличалась между группами и была максимальной в 3-й группе. СКФ (CKD-EPIcys) ниже 60 мл/мин/1,73 м2 была выявлена у 76,7% больных всех групп. СКФ (CKD-EPIcys) статистически значимо отличалась между группами и была минимальной в 3-й группе. При сравнении сывороточного креатинина и цистатина С в 1-й группе у 8 (57,1%) больных выявлена «скрытая» клубочковая дисфункция, которая определяется только по концентрации цистатина С. Отмечена взаимосвязь между уровнем диастолического артериального давления (ДАД) и NGAL (r = 0,44; р &lt; 0,05). Установлены корреляции между показателями диастолической функции левого желудочка (ЛЖ) и показателями фильтрационной функции и канальцевого аппарата почек: между E/e› и концентрацией NGAL (r = 0,31; р &lt; 0,05) и E/e’ и концентрацией цистатина С (r = 0,30; р &lt; 0,05); между E/A и концентрацией NGAL (r = –0,36; р &lt; 0,05) и septal e’ и концентрацией цистатина С (r = –0,30; р &lt; 0,05). Выявлена взаимосвязь между концентрацией NGAL и sST2 (r = 0,44; р &lt; 0,05), а также между концентрацией цистатина С и TIMP-1 (r = 0,39; р &lt; 0,05).</p></sec><sec><title>Заключение</title><p>Заключение. Использование цистатина С в крови для оценки фильтрационной функции почек позволяет выявить «скрытую» клубочковую дисфункцию, неопределяемую по СКФ (CKD-EPIcre), в 57,1% случаев у больных ХСН и персистирующей формой ФП. У больных персистирующей формой ФП формируется ХСН с сохраненной фракцией выброса ЛЖ (ФВ ЛЖ) независимо от фенотипа почечной дисфункции. Степень тяжести как нарушений клубочковой фильтрации, так и канальцевого аппарата почек взаимосвязана с выраженностью диастолической дисфункции. В отличие от клинических показателей и концентрации NT-proBNP в крови sST2 позволяет выявить различия по степени тяжести ХСН у больных персистирующей формой ФП в зависимости от фенотипа ренальной дисфункции: минимальная выраженность – при клубочковой, максимальная – при сочетанной дисфункции. Клубочковая дисфункция у больных ХСН и персистирующей формой ФП ассоциирована с нарушениями процесса коллагенообразования и активацией TIMP-1. </p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Aim</title><p>Aim. To study the features of chronic heart failure (CHF) formation in patients with persistent atrial fibrillation (AF) depending on the phenotype of renal dysfunction.</p></sec><sec><title>Material and Methods</title><p>Material and Methods. The study included 60 patients with persistent AF and CHF. To diagnose CHF, echocardiography study was performed and the concentrations of NT-pRoBNP and sST2 in the blood serum were determined. Renal filtration function was assessed by glomerular filtration rate (GFR) calculated based on creatinine and cystatin C. Plasma NGAL concentration was determined to assess tubular dysfunction. Three phenotypes of renal damage were identified. Group 1 included 14 individuals (23.3%) with isolated tubular dysfunction assessed by NGAL; group 2 included 14 patients (23.3%) with isolated glomerular dysfunction assessed by GFR (CKD-EPIcys); group 3 comprised 32 patients (53.3%) with a combination of tubular and glomerular dysfunction.</p></sec><sec><title>Results</title><p>Results. The GFR value (CKD-EPIcre) below 60 mL/min/1.73 m2 was found in 36.7% of patients from groups 2 and 3. The concentration of cystatin C significantly diff ered between groups and was the highest in group 3. The value of GFR (CKDEPIcys) below 60 mL/min/1.73 m2 was detected in 76.7% of patients from all groups. The value of GFR (CKD-EPIcys) significantly diff ered between groups and was the lowest in group 3. When comparing serum creatinine and cystatin C in group 1, eight patients (57.1%) showed latent glomerular dysfunction, which manifested only in the concentration of cystatin C. A relationship was found between the level of DBP and NGAL (r = 0.44; p &lt; 0.05). The correlations were identified between the parameters of left ventricular (LV) diastolic function and indicators of filtration function and tubular apparatus of the kidneys, namely: between E/e’ and NGAL concentration (r = 0.31; p &lt; 0.05); between E/e’ and cystatin C concentration (r = 0,30; p &lt; 0.05); between E/A and NGAL concentration (r = –0.36; p &lt; 0.05); and between septal e’ and cystatin C concentration (r = –0.30; p &lt; 0.05). Relationships were found between the concentrations of NGAL and sST2 (r = 0.44; p &lt; 0.05) and between the concentrations of cystatin C and TIMP-1 (r = 0.39; p &lt; 0.05).</p></sec><sec><title>Conclusion</title><p>Conclusion. The use of blood cystatin C to assess kidney filtration function allowed to detect latent glomerular dysfunction in 57.1% of patients with heart failure and persistent AF, which could not be determined by GFR (CKD-EPIcre). Patients with persistent AF developed CHF with preserved LV EF regardless of the phenotype of renal dysfunction. The severities of glomerular filtration and kidney tubular apparatus abnormalities correlated with the severity of diastolic dysfunction. Unlike clinical indicators and blood concentration of NT-proBNP, sST2 levels allowed to detect the diff erences in heart failure severity in patients with persistent AF depending on the phenotype of renal dysfunction: the lowest severity was observed in the presence of glomerular dysfunction; the highest severity was found in the presence of combined dysfunction. Glomerular dysfunction in patients with CHF and persistent AF was associated with the impaired collagen formation and TIMP-1 activation. </p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>хроническая сердечная недостаточность</kwd><kwd>клубочковая дисфункция</kwd><kwd>канальцевая дисфункция</kwd><kwd>фибрилляция предсердий</kwd></kwd-group><kwd-group xml:lang="en"><kwd>chronic heart failure</kwd><kwd>glomerular dysfunction</kwd><kwd>tubular dysfunction</kwd><kwd>atrial fibrillation</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">Moe G. Heart failure with multiple comorbidities. Curr. Opin. Cardiol. 2016;31(2):209–216.DOI: 10.1097/HCO.0000000000000257.</mixed-citation><mixed-citation xml:lang="en">Moe G. Heart failure with multiple comorbidities. Curr. Opin. 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