problendoПроблемы ЭндокринологииProblems of Endocrinology0375-96602308-1430Endocrinology Research Centre10.14341/probl13679problendo-13679Research ArticleКлиническая эндокринологияClinical endocrinologyПервичный гиперальдостеронизм как самостоятельный фактор поражения почек. Потенциальные терапевтические стратегии и перспективы исследованийPrimary aldosteronism as an independent factor of kidney damage. Potential therapeutic strategies and research prospectshttps://orcid.org/0000-0001-6388-1544ПлатоноваН. М.PlatonovaN. M.

Платонова Надежда Михайловна - д.м.н.

Москва

Nadezhda M. Platonova - MD, PhD.

Moscow

doc-platonova@inbox.ruhttps://orcid.org/0009-0007-4725-8307ГабибуллаевР. М.GabibullaevR. M.

Габибуллаев Рамазан Максудович

Москва

Ramazan M. Gabibullaev - resident.

Moscow

Ramazan.gab79@mail.ruhttps://orcid.org/0009-0007-0930-5272МахачевД. Р.MakhachevD. R.

Махачев Далгат Рамазанович

117437, Москва, ул. Академика Волгина 37

Dalgat R. Makhachev – student.

37 Akademika Volgina Street, 117437, Moscow

dalgat2002@mail.ruhttps://orcid.org/0009-0006-8420-1468ДотдуевА. А.-Ю.DotduevA. A.-Yu.

Дотдуев Ахмат Абу-Юсуфович

Москва

Akhmat A.-Yu. Dotduev - student.

Moscow

ahmatdotduev@mail.ruhttps://orcid.org/0009-0009-4512-8693ПоляковаД. А.PolyakovaD. A.

Полякова Диана Александровна

Москва

Diana A. Polyakova - student.

Moscow

diana.polyakova.1300@mail.ruhttps://orcid.org/0009-0001-9710-2649МухинаД. А.MukhinaD. A.

Мухина Дарья Александровна

Москва

Daria A. Mukhina - student.

Moscow

muhindara819@gmail.comhttps://orcid.org/0009-0003-8243-5883БельбековаЗ. А.BelbekovaZ. A.

Бельбекова Зарема Анзоровна

Москва

Zarema A. Belbekova – student.

Moscow

zbelbekova@mail.ruhttps://orcid.org/0009-0000-6239-7267МайерВ. В.MayerV. V.

Майер Виолетта Вячеславовна

Москва

Violetta V. Mayer - student.

Moscow

maram003@mail.ruhttps://orcid.org/0009-0002-7447-4770ХадзиевА. С.KhadzievA. S.

Anzor S. Khadziev - student.

Магас

Anzor S. Khadziev - student.

Magas

cor.anzor@gmail.comhttps://orcid.org/0000-0002-8520-8702ТрошинаЕ. А.TroshinaE. A.

Трошина Екатерина Анатольевна - д.м.н., член-корр. РАН, профессор.

Москва

Ekaterina A. Troshina - MD, PhD, Corresponding Member of RAS, Professor.

Moscow

troshina@inbox.ruНМИЦ эндокринологии им. академика И.И. ДедоваРоссияEndocrinology Research CentreRussian FederationРоссийский национальный исследовательский медицинский университет им. Н.И. Пирогова (Пироговский Университет)РоссияPirogov Russian National Research Medical University (Pirogov University), Ministry of Health of the Russian FederationRussian FederationИнгушский государственный университетРоссияIngush State UniversityRussian Federation2026220720267231928Copyright © Платонова Н.М., Габибуллаев Р.М., Махачев Д.Р., Дотдуев А.А., Полякова Д.А., Мухина Д.А., Бельбекова З.А., Майер В.В., Хадзиев А.С., Трошина Е.А., 20262026Платонова Н.М., Габибуллаев Р.М., Махачев Д.Р., Дотдуев А.А., Полякова Д.А., Мухина Д.А., Бельбекова З.А., Майер В.В., Хадзиев А.С., Трошина Е.А.Platonova N.M., Gabibullaev R.M., Makhachev D.R., Dotduev A.A., Polyakova D.A., Mukhina D.A., Belbekova Z.A., Mayer V.V., Khadziev A.S., Troshina E.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.probl-endojournals.ru/jour/article/view/13679

Первичный гиперальдостеронизм (ПГА) — наиболее частая из потенциально излечимых причин вторичной артериальной гипертензии и независимый фактор риска хронической болезни почек (ХБП). Обзор фокусируется на патофизиологических механизмах почечного поражения при ПГА, включая активацию минералокортикоидных рецепторов, негеномные сигнальные пути через GPER, усиление окислительного стресса и экспрессию провоспалительных и профибротических медиаторов (TGF-β1, NF-κB, NLRP3). Показано, что хронический избыток альдостерона инициирует повреждение подоцитов, микроваскулярную дисфункцию и интерстициальный фиброз, приводящие к снижению скорости клубочковой фильтрации и прогрессированию ХБП.

Обсуждаются генетические детерминанты (мутации KCNJ5, ATP1A1, CACNA1D), ассоциированные с более выраженным почечным ремоделированием, и диагностические биомаркеры (L-FABP, KIM-1, микроальбуминурия), отражающие ранние стадии повреждения нефронов. Сравнительный анализ хирургического и медикаментозного лечения демонстрирует, что адреналэктомия обеспечивает более стойкую нефропротекцию, тогда как терапия антагонистами минералокортикоидных рецепторов требует динамического контроля функции почек. Особое внимание уделено новым стратегиям таргетной терапии, включая нестероидные антагонисты и ингибиторы альдостеронсинтазы (баксдростат). Обзор объединяет молекулярные и клинические аспекты альдостерон-индуцированного почечного повреждения, подчеркивая значение ранней диагностики и персонализированных подходов к предотвращению прогрессирования ХБП у пациентов с ПГА.

Primary aldosteronism (PA) is the most common curable cause of secondary hypertension and an independent risk factor for chronic kidney disease (CKD). This review focuses on the pathophysiological mechanisms of aldosterone-induced renal injury, including mineralocorticoid receptor activation, nongenomic signaling via GPER, oxidative stress, and the upregulation of profibrotic and inflammatory mediators such as TGF-β1, NF-κB, and NLRP3. Chronic aldosterone excess leads to podocyte injury, microvascular dysfunction, and interstitial fibrosis, resulting in decreased glomerular filtration rate and CKD progression.

Genetic mutations (KCNJ5, ATP1A1, CACNA1D) and tubular stress biomarkers (L-FABP, KIM-1, microalbuminuria) are discussed as key factors of early nephron injury. Comparative clinical data show that adrenalectomy provides superior nephroprotection compared to pharmacological blockade, while long-term therapy with mineralocorticoid receptor antagonists requires careful renal monitoring. Emerging therapeutic strategies, including nonsteroidal MR antagonists and aldosterone synthase inhibitors (baxdrostat), offer new prospects for targeted nephroprotection.

By integrating molecular and clinical evidence, this review highlights the central role of aldosterone in renal pathology and emphasizes early detection and personalized treatment approaches to prevent CKD progression in patients with PA.

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