nidНефрология и диализNephrology and Dialysis1680-44222618-9801Российское диализное общество10.28996/2618-9801-2019-1-19-31nid-253Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESРоль артериовенозной фистулы в формировании легочной гипертензии у пациентов на заместительной почечной терапии. Обзор литературыThe role of arterio-venous fistula in formation of pulmonary hypertension in patients on renal replacement therapy. A ReviewИсхаковР. Т.IshakovR. T.noemail@neicon.ruЗелтынь-АбрамовЕ. М.Zeltyn-AbramovE. M.ezeltyn@mail.ruПотешкинаН. Г.PotheshkinaN. G.noemail@neicon.ruБелавинаН. И.BelavinaN. I.noemail@neicon.ruФДПО ГБОУ ВПО РНИМУ им. Н.И. Пирогова МЗ РФ; ГБУЗ "ГКБ № 52 Департамента здравоохранения г. Москвы"РоссияPirogov Russian National Research Medical University (RNRMU); Moscow City Hospital 52Russian FederationФДПО ГБОУ ВПО РНИМУ им. Н.И. Пирогова МЗ РФРоссияPirogov Russian National Research Medical University (RNRMU)Russian Federation2019050820242111931Copyright © Исхаков Р.Т., Зелтынь-Абрамов Е.М., Потешкина Н.Г., Белавина Н.И., 20242024Исхаков Р.Т., Зелтынь-Абрамов Е.М., Потешкина Н.Г., Белавина Н.И.Ishakov R.T., Zeltyn-Abramov E.M., Potheshkina N.G., Belavina N.I.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://journal.nephro.ru/jour/article/view/253

Легочная гипертензия (ЛГ) представляет собой сложный патофизиологический и клинический феномен, характеризующийся прогрессирующим повышением давления в легочной артерии (ДЛА). Рост ДЛА может привести к необратимым структурным изменениям легочного сосудистого русла. Клиническим проявлением патоморфологических изменений является формирование тяжелой, часто необратимой, правожелудочковой недостаточности. ЛГ широко распространена среди пациентов с продвинутыми стадиями хронической болезни почек (ХБП), в том числе, получающих заместительную почечную терапию (ЗПТ), являясь независимым предиктором летальности и сердечно-сосудистых осложнений в данной популяции. Патогенетические механизмы формирования ЛГ у пациентов на ЗПТ многообразны и остаются предметом дискуссии. В ряде случаев в качестве причины формирования ЛГ выступают заболевания, коморбидные диализ-потребной ХБП или непосредственно приведшие к ее развитию. Однако в настоящее время внимание экспертов сосредоточено на изучении нейрогуморальных и гемодинамических паттернов развития ЛГ, связанных как с особенностями патоморфоза ХБП, так и с воздействием функционирующей артериовенозной фистулы (АВФ) на центральную гемодинамику. Уточнение гемодинамических аспектов формирования ЛГ у пациентов с АВФ и выработка доказательных лечебных и обсервационных стратегий невозможны без дальнейшего определения влияния АВФ per se на сердечно-сосудистую систему конкретного пациента. Диагностический подход к оценке вероятных клинических сценариев включает в себя этапное эхо-кардиографическое наблюдение, катетеризацию правых отделов сердца, пробу временной окклюзии АВФ. Все диагностические маневры следует проводить с учетом закономерных колебаний волемического статуса пациента, находящегося на программном гемодиализе. Корректная методологическая оценка вклада АВФ в формирование ЛГ позволит сформулировать конкретные лечебные стратегии в диапазоне от реконструкции сосудистого доступа до смены вида ЗПТ.

Pulmonary hypertension (PH) is a complex pathophysiological and clinical phenomenon characterized by a progressive rise of the pulmonary artery pressure (PAP). The rise of PAP may lead to irreversible structural alterations in pulmonary vascular bed. The clinical manifestation of these alterations is severe, often irreversible, right ventricular failure. PH is widespread among patients suffering from advanced stages of chronic kidney disease (CKD), including those who receive renal replacement therapy (RRT). PH is an independent predictor of lethal outcomes and cardiovascular complications in the above-mentioned patient's population. Pathogenetic mechanisms of PH formation in patients on RRT are multiple and still are the subject of discussion. In some cases PH formation is directly associated with a variety of diseases, which are comorbid to dialysis-depended CKD or actually cause CKD itself. However, at the present time, the attention of the expert community is focused on the neurohumoral and hemodynamic patterns of PH formation connected both with specific features of CKD pathomorphosis and the impact of working arterio-venous fistula (AVF) on central hemodynamics. Updating hemodynamic aspects of PH formation in the patients with working AVF and elaborating evidence-based treatment and observational strategies are impossible without further identification of AVF influence per se on cardiovascular system of a given patient. The diagnostic approach to the evaluation of possible clinical scenarios includes serial echocardiographic examinations, right heart catheterization and the test of temporary AVF occlusion. All diagnostic manoeuvers must be provided by taking into account regular fluctuations of volume status of patient on long-term hemodialysis. The proper methodological evaluation of AVF's impact on PH formation will allow defining concrete treatment strategies in the range of vascular access reconstruction to change of RRT modality.

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The authors declare that there are no conflicts of interest present.