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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">cardiovascular</journal-id><journal-title-group><journal-title xml:lang="ru">Кардиоваскулярная терапия и профилактика</journal-title><trans-title-group xml:lang="en"><trans-title>Cardiovascular Therapy and Prevention</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1728-8800</issn><issn pub-type="epub">2619-0125</issn><publisher><publisher-name>«SILICEA-POLIGRAF» LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.15829/1728-8800-2016-1-26-30</article-id><article-id custom-type="elpub" pub-id-type="custom">cardiovascular-312</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>ХРОНИЧЕСКАЯ СЕРДЕЧНАЯ НЕДОСТАТОЧНОСТЬ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CHRONIC HEART FAILURE</subject></subj-group></article-categories><title-group><article-title>Поражение почек у пациентов с хронической сердечной недостаточностью и стеатозом печени</article-title><trans-title-group xml:lang="en"><trans-title>The involvement of kidneys in chronic heart failure patients with liver steatosis</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>Драпкина</surname><given-names>О. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Drapkina</surname><given-names>O. M.</given-names></name></name-alternatives><bio xml:lang="ru"/><email xlink:type="simple">ezyatenkova@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Зятенкова</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Zyatenkov</surname><given-names>E. V.</given-names></name></name-alternatives><bio xml:lang="ru"/><email xlink:type="simple">ezyatenkova@gmail.com</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБУ «Государственный научно-исследовательский центр профилактической медицины» Минздрава России. Москва</institution></aff><aff xml:lang="en"><institution>National Research Center for Preventive Medicine of the Ministry of Health. Moscow</institution></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ГБОУ ВПО «Первый Московский государственный медицинский университет им. И. М. Сеченова» Минздрава России. Москва</institution></aff><aff xml:lang="en"><institution>I.M. Sechenov First Moscow State Medical University of the Ministry of Health. Moscow</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>20</day><month>02</month><year>2016</year></pub-date><volume>15</volume><issue>1</issue><fpage>26</fpage><lpage>30</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Драпкина О.М., Зятенкова Е.В., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Драпкина О.М., Зятенкова Е.В.</copyright-holder><copyright-holder xml:lang="en">Drapkina O.M., Zyatenkov 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://cardiovascular.elpub.ru/jour/article/view/312">https://cardiovascular.elpub.ru/jour/article/view/312</self-uri><abstract><p>В настоящее время в практике врача-интерниста не производится измерение скорости клубочковой фильтрации (СКФ) при отсутствии факторов риска развития хронической болезни почек (ХБП). Однако данные последних исследований показывают, что пациентам с неалкогольной жировой болезнью печени (НАЖБП) необходимо оценить СКФ даже в отсутствие классических факторов риска развития ХБП. Раннее выявление поражения почек у пациентов с хронической сердечной недостаточностью (ХСН) и НАЖБП позволит отобрать больных для дальнейшего обследования и выбора терапии, учитывая сопутствующую патологию.</p><sec><title>Цель</title><p>Цель. Оценить функциональное состояние почек у пациентов с ХСН и стеатозом печени.</p></sec><sec><title>Материал и методы</title><p>Материал и методы. В исследование включены 77 больных с ХСН. У всех пациентов диагноз ХСН подтверждался качественным измерением N-терминального фрагмента мозгового натрийуретического пептида. Оценивались тяжесть клинических проявлений ХСН, функциональный статус пациента. Всем больным проводились клинические и биохимические анализы крови, электрокардиография, ультразвуковое исследование печени. Оценивались размеры камер сердца, толщина стенок миокарда по данным эхокардиографии. Всем больным проводился расчет СКФ по CKD-EPI и определение стадии ХБП, расчет Fatty Liver Index (FLI), NAFLD Fibrosis Score (NFS).</p></sec><sec><title>Результаты</title><p>Результаты. Более половины (66%) пациентов с ХСН имели С2 стадию ХБП, 6% пациентов – С1, 12% – С3а, 9% – С3б, 4% – С4 стадию ХБП. Пациенты с С5 в исследовании отсутствовали. Среднее значение СКФ 65,4±14,4 мл/мин/1,73м2.При статистическом анализе выявлено, что по мере увеличения функционального класса по ШОКС ХСН возрастает стадия ХБП (p=0,0027). Чем выше уровень глюкозы, тем большая стадия ХБП (р=0,0022). Выявлено, что по мере увеличения стадии ХБП у пациентов отмечается увеличение размеров правого предсердия (р=0,044). Чем тяжелее поражение почек у пациентов с ХСН, тем выше уровень маркера фиброза PIIINP миокарда (р=0,047). Согласно FLI у 40% пациентов высокая вероятность наличия стеатоза печени, у 34% пациентов данные о наличии стеатоза печени отсутствовали, 26% пациентов имели промежуточное значение. Согласно NFS 26% пациентов имели высокую вероятность наличия фиброза печени, 9% пациентов – не имели, 65% пациентов находилось в «серой зоне». При анализе взаимосвязей выявлено, что по мере увеличения значения NFS уменьшается значение СКФ, возрастает стадия ХБП (р=0,049).</p></sec><sec><title>Заключение</title><p>Заключение. Пациенты с НАЖБП и ХСН нуждаются в оценке СКФ. Раннее выявление поражения почек у пациентов с ХСН и НАЖБП позволит отобрать больных для дальнейшего обследования и подбора терапии, учитывая сопутствующую патологию.</p></sec></abstract><trans-abstract xml:lang="en"><p>Recently, the internist-practitioner does not routinely assess glomerularfiltration rate (GFR) in there no risk factors for chronic kidney disease(CKD). However, recent data shows that in non-alcoholic fatty liverdisease (NAFLD) it is necessary to assess GFR even without any classicrisk factors for CKD. Early awareness of kidney damage in chronic heartfailure patients (CHF) and NAFLD might help to select those requiringfurther investigation and treatment, taking into account comorbidity.Aim. To assess functional condition of kidneys in CHF patients with liversteatosis.Material and methods. Totally, 77 CHF patients included. All patientshad confirmed CHF diagnosis by N-terminal Brain pro-natriuretic peptideassay. The severity of clinical condition in CHF was assessed, functionalstatus of patient. All patients underwent clinical and biochemical bloodsampling, electrocardiography, ultrasound liver imaging. The heartchambers sizes were assessed, walls thickness by echocardiography. Allpatients had the GFR by CKD-EPI calculated, as the Fatty Liver Index(FLI), NAFLD Fibrosis Score (NFS).Results. More than a half (66%) of patients with CHF had C2 stage ofCKD, 6% — С1, 12% — С3а, 9% — С3б, 4% — С4 stage of CKD. Patients with С5 were absent. Mean GFR was 65,4±14,4 ml/min/1,73 m2. In statistical analysis it was revealed that while there is an increase of SCAHF points, there is parallel increase of CKD stage (p=0,0027). Higher glucose level, higher the stage of CKD (p=0,0022). It was found, that while there is and increase of CKD, right atrium size also increases (p=0,044). With more severe renal damage in CHF, higher the level of PIIINP myocardium fibrosis marker (p=0,047). According to FLI, in 40% of patients there is high chance for liver steatosis, in 34% of patients the data on steatosis was absent, in 26% was intermediate. According to NFS, 26% patients had high probability of liver fibrosis, 9% — did not have, 65% were in a “grey zone”. In analysis of relations there was found that while increasing NFS, GFR does decrease, and CKD stage increases (p=0,049).Conclusion. Patients with NAFLD and CHF do need GFR assessment.Early finding of renal involvement in CHF with NAFLD would help to select patients for further investigation and therapy prescription, taking into account comorbidity.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>хроническая сердечная недостаточность</kwd><kwd>хроническая болезнь почек</kwd><kwd>N-терминальный пропептид коллагена III типа</kwd><kwd>Fatty Liver Index</kwd><kwd>NAFLD Fibrosis Score</kwd></kwd-group><kwd-group xml:lang="en"><kwd>chronic heart failure</kwd><kwd>chronic kidney disease</kwd><kwd>N-terminal propetide of collagen III type</kwd><kwd>Fatty Liver Index</kwd><kwd>NAFLD Fibrosis Score.</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">Renal function and prediction of cardiovascular risk. Russian guidelines. Cardiovascular Therapy and Prevention 2008; 7(6): 41, Suppl. 3. 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