nefrНефрологияNephrology (Saint-Petersburg)1561-62742541-9439Pavlov First Saint-Petersburg State Medical University10.36485/1561-6274-2020-24-1-9-21nefr-1786Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESНекоторые причины развития протеинурии при нефротическом синдромеSeveral reasons for the development of proteinuria in nephrotic syndromehttps://orcid.org/0000-0002-8101-103XЗверевЯ. Ф.ZverevYa. F.

Зверев Яков Федорович, профессор, доктор медицинских наук, кафедра фармакологии

656038, г. Барнаул, пр. Ленина, д. 40.

Prof. Yakov F. Zverev, MD, PhD, DMedSci, Department of Pharmacology.

: 656038, Russia, Barnaul, Lenin avenue, 40

zver@agmu.ruhttps://orcid.org/0000-0002-5889-7071РыкуноваА. Я.RykunovaA. Ya.

Рыкунова Анна Яковлевна, кандидат медицинских наук, кафедра криминалистики

656038, г. Барнаул, ул. Чкалова, д. 49

Anna Ya. Rykunova, MD, Department of Criminology.

656038, Russia, Barnaul, Chkalov st., 49.

zveranna@mail.ruАлтайский государственный медицинский университетРоссияAltai State Medical UniversityRussian FederationБарнаульский юридический институтРоссияBarnaul Law InstituteRussian Federation202023012020241921Copyright © Зверев Я.Ф., Рыкунова А.Я., 20202020Зверев Я.Ф., Рыкунова А.Я.Zverev Y.F., Rykunova A.Y.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://journal.nephrolog.ru/jour/article/view/1786

В обзоре рассматриваются некоторые причины возникновения протеинурии при нефротическом синдроме, обусловленные внепочечными механизмами. Отмечены идентифицированные в последние годы аутоантитела, участвующие в нарушении селективной проницаемости фильтрационного барьера при мембранозной нефропатии. Анализируется прямая связь между уровнем гипергликемии и протеинурией при диабетической нефропатии. Подчеркивается роль в развитии этого заболевания активных форм кислорода, конечных продуктов гликирования, ангиотензина II, трансформирующего фактора роста β-1, эпителиально-мезенхимальной трансформации подоцитов, Rho ГТФаз, внутриклеточного сигнального пути mTOR, Wnt/β-катенин сигнального каскада. Особое внимание уделено проблеме поиска и идентификации циркулирующих факторов проницаемости в патогенезе идиопатического нефротического синдрома при болезни минимальных изменений и фокально-сегментарном гломерулосклерозе: фактор сосудистой проницаемости (VPF), вазодилататор-стимулированный фосфопротеин (VASP), гемопексин (Hpx), растворимый активатор рецептора плазминогена уриказного типа (suPAR), кардиотропиноподобный цитокин-1 (CLCF-1) и анти-CD40 антитела. Отмечено, что роль таких факторов сегодня не подвергается сомнению, однако с позиций доказательной медицины эта роль нуждается в серьезном подтверждении в соответствии со специально сформулированными критериями.

The review discusses some of the causes of proteinuria in nephrotic syndrome due to extrarenal mechanisms. Autoantibodies identified in recent years are involved in the violation of the selective permeability of the filtration barrier in membranous nephropathy. The direct relationship between the level of hyperglycemia and proteinuria in diabetic nephropathy is analyzed. The role of reactive oxygen species, end products of glycation, angiotensin II, transforming growth factor β-1, epithelial-mesenchymal transformation of podocytes, Rho GTPases, intracellular signaling pathway mTOR, Wnt/β-catenin signaling cascade is emphasized. Particular attention is paid to the problem of searching and identifying circulating permeability factors in the pathogenesis of idiopathic nephrotic syndrome in patients with minimal changes and focal segmental glomerulosclerosis: vascular permeability factor (VPF), vasodilator-stimulated phosphoprotein (VASP), soluble hemopexin (Hpx) receptor-receptor-receptor type (suPAR), cardiotropin-like cytokine-1 (CLCF-1) and anti-CD40 antibodies. It is noted that the role of such factors is not in doubt today, however, from the standpoint of evidence-based medicine, this role needs serious confirmation by specially formulated criteria.

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