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<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="review-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">The Clinician</journal-id><journal-title-group><journal-title xml:lang="en">The Clinician</journal-title><trans-title-group xml:lang="ru"><trans-title>Клиницист</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1818-8338</issn><issn publication-format="electronic">2412-8775</issn><publisher><publisher-name xml:lang="en">Publishing House ABV Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">690</article-id><article-id pub-id-type="doi">10.17650/1818-8338-2025-19-4-K760</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>REVIEW</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>ОБЗОР</subject></subj-group><subj-group subj-group-type="article-type"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Pulmonary hypertension in patients with chronic kidney disease: the multifaceted pathogenesis</article-title><trans-title-group xml:lang="ru"><trans-title>Легочная гипертензия у пациентов с хронической болезнью почек: многогранность патогенеза</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-8266-6022</contrib-id><name-alternatives><name xml:lang="en"><surname>Andriyashkina</surname><given-names>Darya Yu.</given-names></name><name xml:lang="ru"><surname>Андрияшкина</surname><given-names>Дарья Юрьевна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>andryashkina.darya@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0005-6472-300X</contrib-id><name-alternatives><name xml:lang="en"><surname>Podoprigora</surname><given-names>V. V.</given-names></name><name xml:lang="ru"><surname>Подопригора</surname><given-names>В. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>andryashkina.darya@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0001-4162-6013</contrib-id><name-alternatives><name xml:lang="en"><surname>Kamyshev</surname><given-names>S. S.</given-names></name><name xml:lang="ru"><surname>Камышев</surname><given-names>С. С.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>andryashkina.darya@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7410-9784</contrib-id><name-alternatives><name xml:lang="en"><surname>Klimenko</surname><given-names>Alesya A.</given-names></name><name xml:lang="ru"><surname>Клименко</surname><given-names>Алеся Александровна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>MD, PhD, Associate Professor, Head of the Department of Acad. A.I. Nesterov of Faculty Therapy</p></bio><bio xml:lang="ru"><p>д.м.н., доцент, заведующая кафедрой факультетской терапии им. акад. А.И. Нестерова Института клинической медицины</p></bio><email>andryashkina.darya@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">N. I. Pirogov Russian National Research Medical University, Ministry of Health of Russia</institution></aff><aff><institution xml:lang="ru">ФГАОУ ВО «Российский национальный исследовательский медицинский университет им. Н. И. Пирогова» Минздрава России</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2026-03-17" publication-format="electronic"><day>17</day><month>03</month><year>2026</year></pub-date><volume>19</volume><issue>4</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>43</fpage><lpage>52</lpage><history><date date-type="received" iso-8601-date="2026-03-16"><day>16</day><month>03</month><year>2026</year></date><date date-type="accepted" iso-8601-date="2026-03-16"><day>16</day><month>03</month><year>2026</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2026, Andriyashkina D.Y., Podoprigora V.V., Kamyshev S.S., Klimenko A.А.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2026, Андрияшкина Д.Ю., Подопригора В.В., Камышев С.С., Клименко А.А.</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="en">Andriyashkina D.Y., Podoprigora V.V., Kamyshev S.S., Klimenko A.А.</copyright-holder><copyright-holder xml:lang="ru">Андрияшкина Д.Ю., Подопригора В.В., Камышев С.С., Клименко А.А.</copyright-holder><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://klinitsist.abvpress.ru/Klin/article/view/690">https://klinitsist.abvpress.ru/Klin/article/view/690</self-uri><abstract xml:lang="en"><p>Pulmonary hypertension (PH) is a group of diseases characterized by progressive increase in pulmonary vascular resistance, which leads to development of right ventricular failure and an unfavorable prognosis of life. There are 5 groups in the clinical classification, mainly based on the cause and pathophysiological changes in the pulmonary vessels. PH in patients with chronic kidney disease (CKD) is a common and severe complication and belongs to group 5 in the classification. PH is diagnosed in 21 % of patients with CKD who are not on dialysis and in 50–60 % of patients with end-stage kidney disease. On the other hand, development of CKD in patients with pulmonary hypertension doubles the risk of mortality, and with end-stage CKD it triples. In most patients in this group, the main causes of PH are volume overload and left ventricular dysfunction. However, many other factors both enhance and offset the effect of volume overload on PH. These factors include the effects of vascular access for dialysis, anemia, respiratory disorders and hypoxemia, inflammation, and changes in mineral metabolism. In addition, CKD can directly affect the blood vessels of the lungs through the action of nitric oxide, endothelin-1, prostacyclin. Catheterization of the right heart, as the basis for the diagnosis of PH, provides insight into the potential hemodynamic profile of pulmonary hypertension associated with CKD. The article summarizes current data undelying new theoretical mechanisms of pathogenesis of PH associated with CKD.</p></abstract><trans-abstract xml:lang="ru"><p>Легочная гипертензия (ЛГ) – группа заболеваний, характеризующихся прогрессирующим повышением легочного сосудистого сопротивления, которое приводит к развитию правожелудочковой сердечной недостаточности и неблагоприятному прогнозу жизни. В клинической классификации выделяют 5 групп ЛГ, в основном опираясь на причину возникновения и патофизиологические изменения легочных сосудов. ЛГ у пациентов с хронической болезнью почек (ХБП) является распространенным и тяжелым осложнением и в классификации относится к 5-й группе. ЛГ диагностируется у 21 % пациентов с ХБП, не находящихся на диализе, и у 50–60 % пациентов с терминальной стадией заболевания почек. В случае развития ХБП у пациентов с ЛГ риск смертности удваивается, в терминальной стадии ХБП – утраивается. У большинства пациентов в этой группе основными причинами ЛГ являются объемная перегрузка и дисфункция левого желудочка. Однако множество других факторов как усиливают, так и нивелируют влияние объемной перегрузки на ЛГ. Эти факторы включают в себя влияние сосудистого доступа для диализа, анемию, нарушения дыхания и гипоксемию, воспаление и изменение минерального обмена. Кроме того, ХБП может непосредственно влиять на сосуды легких посредством действия оксида азота, эндотелина-1 и простациклина. Катетеризация правых отделов сердца как основа диагностики ЛГ позволяет получить представление о потенциальном гемодинамическом профиле ЛГ, связанной с ХБП. В статье обобщены современные данные, представляющие новые теоретические механизмы патогенеза ЛГ, ассоциированной с ХБП.</p></trans-abstract><kwd-group xml:lang="en"><kwd>pulmonary hypertension</kwd><kwd>chronic kidney disease</kwd><kwd>hemodynamic variant</kwd><kwd>hemodialysis</kwd><kwd>arteriovenous fistula</kwd><kwd>calciprotein particle</kwd><kwd>phosphaturic hormone</kwd><kwd>endothelin-1 receptor antagonist</kwd><kwd>nitric oxide</kwd><kwd>prostacyclin</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>легочная гипертензия</kwd><kwd>хроническая болезнь почек</kwd><kwd>гемодинамический вариант</kwd><kwd>гемодиализ</kwd><kwd>артериовенозный шунт</kwd><kwd>кальций-протеиновая частица</kwd><kwd>фосфатурический гормон</kwd><kwd>антагонист рецепторов эндотелина-1</kwd><kwd>оксид азота</kwd><kwd>простациклин</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Simonneau G., Montani D., Celermajer D.S. et al. 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