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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">10.24884/1561-6274-2009-13-1-15-20</article-id><article-id custom-type="elpub" pub-id-type="custom">nefr-1144</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>ПЕРЕДОВАЯ СТАТЬЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>LEADING ARTICLE</subject></subj-group></article-categories><title-group><article-title>ПРОРЕНИН И РЕНИН – НОВЫЕ МИШЕНИ ДЛЯ РЕНО- И КАРДИОПРОТЕКТИВНОЙ ТЕРАПИИ</article-title><trans-title-group xml:lang="en"><trans-title>PRORENIN AND RENIN – NEW TARGETS FOR RENO- AND CARDIOPROTECTIVE THERAPY</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 институт нефрологии</p><p>197022 Санкт-Петербург, ул. Л. Толстого 17, НИИ Нефрологии СПбГМУ им. акад. И.П. Павлова; тел.: (812)-234-01-65</p></bio><email xlink:type="simple">smirnov@nephrolog.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>Смирнов</surname><given-names>К. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Smirnov</surname><given-names>K. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Научно-исследовательский институт нефрологии</p><p>197022 Санкт-Петербург, ул. Л. Толстого 17</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff xml:lang="ru" id="aff-1"><institution>Санкт-Петербургский государственный медицинский университет имени академика И.П. Павлова</institution><country>Russian Federation</country></aff><pub-date pub-type="collection"><year>2009</year></pub-date><pub-date pub-type="epub"><day>10</day><month>01</month><year>2009</year></pub-date><volume>13</volume><issue>1</issue><fpage>15</fpage><lpage>20</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Смирнов А.В., Смирнов К.А., 2009</copyright-statement><copyright-year>2009</copyright-year><copyright-holder xml:lang="ru">Смирнов А.В., Смирнов К.А.</copyright-holder><copyright-holder xml:lang="en">Smirnov A.V., Smirnov K.A.</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/1144">https://journal.nephrolog.ru/jour/article/view/1144</self-uri><abstract><p>Имеющиеся на сегодняшний день экспериментальные данные дают основание предполагать, что в условиях блокады ангиотензипревращающего фермента (АПФ) и АТ₁ - рецепторов к ангиотензину II (А-II), проренин и ренин могут проявлять свою профибротическую активность, действуя через специфический проренин/рениновый (П/Р) рецептор. Профибротический эффект проренин/ренина, хотя и обнаружен в основном в почечной ткани, не может считаться изолированным патофизиологическим феноменом и П/Р могут связываться со специфическим рецептором на поверхности кардиомиоцита. В настоящее время проходит клинические испытания новый препарат, единственный представитель группы прямых ингибиторов ренина-алискирен (aliskirеn), недавно одобренный комитетом FDA США в качестве препарата для лечения артериальной гипертензии. Однако до настоящего времени остается неясным вопрос, насколько клинически значимой окажется блокада (про) рениновых рецепторов в отношении развития почечного и сердечного фиброза. Предварительные данные клинических исследований алискирена обнадеживают: уровень микроальбуминурии в ходе его применения снижается на 61% по сравнению с 50% на фоне применения рамиприла. В настоящее время продолжаются два клинических исследования III фазы по оценке эффективности лечения алискиреном больных с хронической болезнью почек (ХБП): AVOID (Aliskiren in the Evaluation of Proteinuria in Diabetes) и AZTITUDE (Aliskiren Trial in Type 2 Diabetic Nephropathy). Результаты этих исследований должны дать новую информацию о влиянии терапии алискиреном на частоту и тяжесть осложнений диабета. Таким образом, открытие новых механизмов функционирования и значения ренин-ангиотензин-альдостероновой системы, по-видимому, в скором будущем создаст новые предпосылки к совершенствованию рено- и кардиопротективной терапии.</p></abstract><trans-abstract xml:lang="en"><p>The today experimental data give us a reason to propose that in the case of the block of angiotensineconverting enzyme (ACE) and AT₁ – receptors to angiotensin II (A-II), prorenin and renin can show their profibrotic activity, acting through a specific prorenin/renin receptor. The profibrotic effect of prorenin/renin, even though mostly is noticed in the renal tissue, can cot be considered an isolated pathophysiological phenomena and P/R can connect with specific receptors on the surface of cardiomiocyte. At the present time take placethers clinical investigations of a new agent, which is the only representative of the direct inhibitors group of renin-aliskiren, which recently was approved by the FDA committee in USA as a medicine for arterial hypertension treatment. However, until present time it is not clear how much is the clinical significant is the blockade of (pro) renin receptors in accordance with the renal and cardiac fibrosis. The data of previous clinical investigations of aliskiren are very inspiring: the microalbumine level during its use decreases on 61% as compared with 50% during the ramipril intake. At present time take place two clinical investigations of the III phase on the evaluating the efficiency of aliskiren treatment in patients with chronic kidney disease (CKD): AVOID (Aliskiren in the Evaluation of Proteinuria in Diabetes) and AZTITUDE (Aliskiren Trial in Type 2 Diabetic Nephropathy). The results of these investigations should give new information on the therapy influence of aliskiren on the frequency and severityof diabetes. In such way, the opening of new mechanisms of functioning and meaning of renin – angiotensin- aldosterone system, probably shortly will have new ways of innovating reno- and cardioprotective therapy.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>ренин-ангиотензин-альдостероновая система</kwd><kwd>проренин</kwd><kwd>ренин</kwd><kwd>рецепторы ренина</kwd><kwd>алискирен</kwd></kwd-group><kwd-group xml:lang="en"><kwd>renin-angiotensin-aldosteron system</kwd><kwd>prorenin</kwd><kwd>renin</kwd><kwd>renin receptors</kwd><kwd>aliskiren</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">Ruster C, Wolf G. Renin- angiotensin- aldosteron system and progression of renal disease. J Am Soc Nephrol 2006; 17: 2985-2991</mixed-citation><mixed-citation xml:lang="en">Ruster C, Wolf G. Renin- angiotensin- aldosteron system and progression of renal disease. 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