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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">nefr</journal-id><journal-title-group><journal-title xml:lang="ru">Нефрология</journal-title><trans-title-group xml:lang="en"><trans-title>Nephrology (Saint-Petersburg)</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1561-6274</issn><issn pub-type="epub">2541-9439</issn><publisher><publisher-name>Pavlov First Saint-Petersburg State Medical University</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.24884/1561-6274-2005-9-3-81-87</article-id><article-id custom-type="elpub" pub-id-type="custom">nefr-686</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>ЭКСПЕРИМЕНТАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group></article-categories><title-group><article-title>ГОМОЦИСТЕИН ВЫЗЫВАЕТ ПОВРЕЖДЕНИЯ НЕ ТОЛЬКО КЛУБОЧКОВОГО, НО И КАНАЛЬЦЕВОГО ОТДЕЛА НЕФРОНА (ЭКСПЕРИМЕНТАЛЬНОЕ ИССЛЕДОВАНИЕ)</article-title><trans-title-group xml:lang="en"><trans-title>HOMOCYSTEIN CAUSES LESIONS OF NOT ONLY GLOMERULAR BUT ALSO TUBULAR PART OF THE NEPHRON (EXPERIMENTAL STUDY)</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>Смирнов</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Smirnov</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Научно-исследовательский центр, кафедра патологической физиологии</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Добронравов</surname><given-names>В. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Dobronravov</surname><given-names>V. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Научно-исследовательский центр, кафедра патологической физиологии</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Неворотин</surname><given-names>А. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Nevorotin</surname><given-names>A. I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Научно-исследовательский центр, кафедра патологической физиологии</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Хохлов</surname><given-names>С. Е.</given-names></name><name name-style="western" xml:lang="en"><surname>Khokhlov</surname><given-names>S. E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Научно-исследовательский центр, кафедра патологической физиологии</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Сиповский</surname><given-names>В. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Sipovsky</surname><given-names>V. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Научно-исследовательский центр, кафедра патологической физиологии</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Барабанова</surname><given-names>В. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Barabanova</surname><given-names>V. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Научно-исследовательский центр, кафедра патологической физиологии</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Чефу</surname><given-names>С. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Chefu</surname><given-names>S. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Научно-исследовательский центр, кафедра патологической физиологии</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Жлоба</surname><given-names>А. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Zhloba</surname><given-names>A. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Научно-исследовательский центр, кафедра патологической физиологии</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Блашко</surname><given-names>Э. Л.</given-names></name><name name-style="western" xml:lang="en"><surname>Blashko</surname><given-names>E. L.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Научно-исследовательский центр, кафедра патологической физиологии</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff xml:lang="ru" id="aff-1"><institution>Научно-исследовательский институт нефрологии, Cанкт-Петербургский государственный медицинский университет имени акад. И.П. Павлова</institution><country>Russian Federation</country></aff><pub-date pub-type="collection"><year>2005</year></pub-date><pub-date pub-type="epub"><day>10</day><month>03</month><year>2005</year></pub-date><volume>9</volume><issue>3</issue><fpage>81</fpage><lpage>87</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Смирнов А.В., Добронравов В.А., Неворотин А.И., Хохлов С.Е., Сиповский В.Г., Барабанова В.В., Чефу С.Г., Жлоба А.А., Блашко Э.Л., 2005</copyright-statement><copyright-year>2005</copyright-year><copyright-holder xml:lang="ru">Смирнов А.В., Добронравов В.А., Неворотин А.И., Хохлов С.Е., Сиповский В.Г., Барабанова В.В., Чефу С.Г., Жлоба А.А., Блашко Э.Л.</copyright-holder><copyright-holder xml:lang="en">Smirnov A.V., Dobronravov V.A., Nevorotin A.I., Khokhlov S.E., Sipovsky V.G., Barabanova V.V., Chefu S.G., Zhloba A.A., Blashko E.L.</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.nephrolog.ru/jour/article/view/686">https://journal.nephrolog.ru/jour/article/view/686</self-uri><abstract><p>ЦЕЛЬЮ ИССЛЕДОВАНИЯ было выявление функциональных и структурных последствий экспериментальной гипергомо цистеинемии в почках крыс. МАТЕРИАЛ И МЕТОДЫ. Взрослым белым крысам линии Вистар в течение 3 недель паренте рально вводили гомоцистеин (ГЦ; 13.4 мг/кг) для оценки влияния экспериментальной гипергомоцистеинемии (ГГЦ) на мочевую экскрецию альбумина (МЭА), клиренс креатинина (CCr), а также на структуры клубочков и проксимальных каналь цев (ПК) на светооптическом и электронномикроскопическим уровнях. РЕЗУЛЬТАТЫ. Развитие умеренной ГГЦ у экспери ментальных животных приводило к достоверному увеличению МЭА без достоверного изменения CCr, что сопровождалось умеренной мезангиальной пролиферацией, гиперплазией гломерулярной базальной мембраны, заметным увеличением числа больших апикальных вакуолей и вторичных лизосом, а также очаговой утратой щеточной каймы в отдельных клетках ПК. Кроме того, в ПК было отмечено увеличение количества аутофагосом, наряду с наличием эпителиальных клеток с дезорганизованными участками базальной цитоплазмы. ЗАКЛЮЧЕНИЕ. Полученные данные следует рассматривать как прямое доказательство повреждающего действия ГГЦ на клубочки и клетки ПК.</p></abstract><trans-abstract xml:lang="en"><p>THE AIM of the investigation was to find out the functional and structural consequences of experimental hyperhomocysteinemia (hHcy) in the rats’ kidneys. MATERIAL AND METHODS. Adult albino Wistar rats were exposed to daily parenteral homocysteine for three weeks in order to evaluate the influence of experimental hHcy on urinary albumine excretion (UAE), plasma creatinine concentration and creatinine clearance (CCr) as well as on the alterations of the glomerular and proximal tubular (PT) structures at the light and electron microscopy levels. RESULTS. The development of mild hHcy in experimental animals resulted in significantly increased UAE without a significant CCr change that was accompanied by moderate focal mesangial and endothelial cell proliferation, glomerular basement membrane hyperplasia, appreciably increased number of large apical vacuoles and secondary lysosomes, and focal loss of the brush border in certain PT cells. In addition, an increased number of autophagic vacuoles along with the epithelial cells with disorganized loci of the basal cytoplasm was noted. CONCLUSION. The data obtained are considered to be a direct evidence of the impairing effect of hHcy on the glomeruli and PT cells.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>гомоцистеин</kwd><kwd>почки</kwd><kwd>повреждения</kwd></kwd-group><kwd-group xml:lang="en"><kwd>homocysteine</kwd><kwd>kidneys</kwd><kwd>lesions</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">Miller A, Mujumdar V, Shek E et al. Hyperhomocyst(e)inemia induces multiorgan damage. Heart Vessels 2000;15(3):135143</mixed-citation><mixed-citation xml:lang="en">Miller A, Mujumdar V, Shek E et al. Hyperhomocyst(e)inemia induces multiorgan damage. Heart Vessels 2000;15(3):135143</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Li N, Chen YF, Zou AP. Implications of hyperhomocysteinemia in glomerular sclerosis in hypertension. 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