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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">nid</journal-id><journal-title-group><journal-title xml:lang="ru">Нефрология и диализ</journal-title><trans-title-group xml:lang="en"><trans-title>Nephrology and Dialysis</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1680-4422</issn><issn pub-type="epub">2618-9801</issn><publisher><publisher-name>Российское диализное общество</publisher-name></publisher></journal-meta><article-meta><article-id custom-type="elpub" pub-id-type="custom">nid-450</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>ОБЗОРЫ И ЛЕКЦИИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS AND LECTURES</subject></subj-group></article-categories><title-group><article-title>Нефротический синдром: роль ангиопоэтинов в патогенезе</article-title><trans-title-group xml:lang="en"><trans-title>Nephrotic syndrome: role of the angiopoietins in the pathogenesis</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>Ермоленко</surname><given-names>В. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Ermolenko</surname><given-names>V. M.</given-names></name></name-alternatives><email xlink:type="simple">nephrology@mail.ru</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>Филатова</surname><given-names>Н. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Filatova</surname><given-names>N. N.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ГБОУ ДПО РМАПО Минздрава РФ</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Russian Medical Academy of postgraduate education, Russiаn Ministry of health</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>19</day><month>08</month><year>2024</year></pub-date><volume>18</volume><issue>4</issue><fpage>387</fpage><lpage>393</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Ермоленко В.М., Филатова Н.Н., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Ермоленко В.М., Филатова Н.Н.</copyright-holder><copyright-holder xml:lang="en">Ermolenko V.M., Filatova N.N.</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://journal.nephro.ru/jour/article/view/450">https://journal.nephro.ru/jour/article/view/450</self-uri><abstract><p>Сосудистые эндотелиальные факторы роста, обеспечивающие ангио- и васкулогенез, играют важнейшую роль в физиологии и патологии человека. Влияя на функции эндотелия, ангиопоэтины способствуют образованию первичных кровеносных сосудов у эмбриона, а у взрослых способствуют заживлению ран, улучшают коллатеральную циркуляцию при инфаркте миокарда, ускоряя реабилитацию пациентов. В то же время ангиопоэтины индуцируют целый ряд неблагоприятных эффектов: развитие диабетической ретинопатии, макулярной дегенерации сетчатки, ускоряют рост и метастазирование злокачественных опухолей. В обзоре приводятся данные о роли агиопоэтинов (VEGF-A и ANGPTL4) в патогенезе основных проявлений нефротического синдрома - протеинурии, отеков, дислипидемии. Установлено, что экспрессия гипосиализированной формы ANGPTL4 в подоцитах способна вызывать развитие нефротического синдрома и гипертриглицеридемии у больных диабетической нефропатией и гломерулонефритом с минимальными изменениями. Однако на фоне продолжающихся потерь белка с мочой повышается экспрессия ANGPTL4 в сердце, печени, мышцах, уменьшающая протеинурию, но одновременно усугубляющая гипертриглицеридемию. В то же время мутантные формы ANGPTL4 индуцируют ремиссию нефротического синдрома, не ухудшая липидный профиль. Назначение больным N-ацетил-D-маннозамина способно трансформировать гипосиализированный ANGPTL4 в нормальный и существенно снижать протеинурию и предупреждать рецидивы нефротического синдрома.</p></abstract><trans-abstract xml:lang="en"><p>Vascular endothelial growth factors which promote angiogenesis and vasculogenesis play a major role in human physiology and pathology. They affect the function of the endothelium, promote angiopoietins in the fetus, contribute to the formation of the primary blood vessels and in adults, contribute to the healing of wounds, improve collateral circulation in myocardial infarction and accelerate the rehabilitation of patients. At the same time, angiopoietins induces a number of adverse effects: progression of diabetic retinopathy, macular degeneration of the retina, accelerate growth and metastasis of cancer. This review presents data on the role of angiopoietins (VEGF-A, ANGPTL4) in the pathogenesis of the major manifestations of nephrotic syndrome - proteinuria, oedema, dyslipidaemia. It was demonstrated that the expression of hyposialylized of ANGPTL4 in podocytes is capable to induce the development of nephrotic syndrome in the patients with diabetic nephropathy and minimal changes glomerulonephritis. However, with continued loss of protein in the urine increases of expression of ANGPTL4 in the heart, liver, muscles and reduces proteinuria, but exacerbates hypertriglyceridemia. However, the mutant forms of ANGPTL4 are capable to induce a remission of nephrotic syndrome without degrading of the lipid profile. Prescription of N-acetyl-D-mannosamine to patients with nephrotic syndrome is able to transform hyposialylized ANGPTL4 into a normal ANGPTL4, significantly reduce proteinuria and prevent recurrence of nephrotic syndrome.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>нефротический синдром</kwd><kwd>сосудистые эндотелиальные факторы роста</kwd><kwd>ангиопоэтины</kwd><kwd>nephrotic syndrome</kwd><kwd>vascular endothelial growth factor</kwd><kwd>angiopoietins</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">Andersen H, Friis UG, Hansen PB et al. Diabetic nephropathy is associated with increased urine excretion of proteases plasmin, prostasin and urokinase and activation of amiloride-sensitive current in collecting duct cells. Nephrol Dial Transplant. 2015. 30(5): 781-9.</mixed-citation><mixed-citation xml:lang="en">Andersen H, Friis UG, Hansen PB et al. 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