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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">10.24884/1561-6274-2019-23-4-96-111</article-id><article-id custom-type="elpub" pub-id-type="custom">nefr-1728</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>ПРОГРАММА НЕПРЕРЫВНОГО ПОСЛЕДИПЛОМНОГО ОБРАЗОВАНИЯ ПО НЕФРОЛОГИИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>PROGRAM ON CONTINUOUS POSTGRADUATE EDUCATION ON NEPHROLOGY</subject></subj-group></article-categories><title-group><article-title>Нарушения клубочкового фильтрационного барьера как причина протеинурии при нефротическом синдроме</article-title><trans-title-group xml:lang="en"><trans-title>Disorders of club filtration barrier as the cause of proteinuria in the nephrotic syndrome</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8101-103X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Зверев</surname><given-names>Я. Ф.</given-names></name><name name-style="western" xml:lang="en"><surname>Zverev</surname><given-names>Ya. F.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Зверев Яков Федорович - докор медицинских наук, профессор, кафедра фармакологии.</p><p>656038, Барнаул, пр. Ленина, д. 40, Тел.: 8(3852)566-891</p></bio><bio xml:lang="en"><p>Yakov F. Zverev - MD, DMedSci, Prof., Department of Pharmacology.</p><p>656038, Barnaul, Lenin avenue, 40, Phone: 8(3852)566-891</p></bio><email xlink:type="simple">zver@agmu.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-5889-7071</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Рыкунова</surname><given-names>А. Я.</given-names></name><name name-style="western" xml:lang="en"><surname>Rykunova</surname><given-names>A. Ya.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Рыкунова Анна Яковлевна - кандидат медицинских наук, кафедра криминалистики.</p><p>656038, Барнаул, ул. Чкалова, д. 49, Тел.: 8 (3852) 379-163</p></bio><bio xml:lang="en"><p>Anna Ya. Rykunova - MD, PhD, Department of Criminology.</p><p>656038, Barnaul, Chkalov st., 49, Phone: 8(3852)379163</p></bio><email xlink:type="simple">zveranna@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Алтайский государственный медицинский университет</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Altai State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Барнаульский юридический институт</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Barnaul Law Institute</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2019</year></pub-date><pub-date pub-type="epub"><day>23</day><month>06</month><year>2019</year></pub-date><volume>23</volume><issue>4</issue><fpage>96</fpage><lpage>111</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Зверев Я.Ф., Рыкунова А.Я., 2019</copyright-statement><copyright-year>2019</copyright-year><copyright-holder xml:lang="ru">Зверев Я.Ф., Рыкунова А.Я.</copyright-holder><copyright-holder xml:lang="en">Zverev Y.F., Rykunova A.Y.</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/1728">https://journal.nephrolog.ru/jour/article/view/1728</self-uri><abstract><p>Обзор посвящен причинам и механизмам возникновения протеинурии при различных заболеваниях, сопровождающихся развитием нефротического синдрома. Проанализирован вклад повреждений основных компонентов клубочкового фильтрационного барьера, включая эндотелий клубочковых капилляров, гломерулярную базальную мембрану и подоциты. Показано, что индукция протеинурии может быть следствием нарушений структуры и функции каждого из названных слоев фильтра, как и его комбинированного повреждения. Уделено особое внимание роли гликокалик-са и его составляющих, а также активных форм кислорода и эндотелиального фактора роста в патогенезе нарушений селективной проницаемости эндотелия капилляров почечных клубочков при болезни минимальных изменений, фокально-сегментарном гломерулосклерозе, преэклампсии, диабетогенной нефропатии. Обсуждается значимость таких генетических нарушений гломерулярной мембраны, как синдромы Пирсона, Альпорта. Отдельно рассматриваются также генные мутации, обусловливающие нарушения структуры и функционирования основных белков актино-вого цитоскелета подоцитов.</p></abstract><trans-abstract xml:lang="en"><p>The review is devoted to the causes and mechanisms of proteinuria in various diseases associated with the development of the nephrotic syndrome. The contribution of damage to the main components of the glomerular filtration barrier, including the endothelium of glomerular capillaries, glomerular basement membrane, and podocytes, was analyzed. It is shown that the induction of proteinuria may be a consequence of disorders of the structure and function of each of these layers of the filter, as well as its combined damage. Special attention is given to the role of the glycocalyx and its components as well as reactive oxygen species and endothelial growth factor in the pathogenesis of disorders of the selective permeability of the capillary endothelium of the glomeruli in minimal change disease, focal segmental glomerulosclerosis, pre-eclampsia, diabetogenic nephropathy. The significance of such genetic disorders of the glomerular membrane as Pearson and Alport syndromes is discussed. Gene mutations causing disorders of the structure and functioning of the main proteins of the actinic cytoskeleton of podocytes are considered separately.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>клубочковый фильтрационный барьер</kwd><kwd>эндотелий клубочковых капилляров</kwd><kwd>базальная мембрана</kwd><kwd>подоциты</kwd><kwd>протеинурия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>glomerular filtration barrier</kwd><kwd>endothelium of glomerular capillaries</kwd><kwd>basal membrane</kwd><kwd>podocytes</kwd><kwd>proteinuria</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">Тареева ИЕ, Полянцева ЛР Протеинурия и нефротический синдром. В: Тареева ИЕ, ред. Нефрология. Руководство для врачей. Медицина, М., 2000; 145-150</mixed-citation><mixed-citation xml:lang="en">Tareeva IE, Polyantseva LR.Proteinurija i nefroticheskij syndrom. V: Tareeva IE, red. Nefrologija. Rukovodstvodlya vrachej. Meditsina, M., 2000; 145-150 (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Сахаров ИВ, Сукало АВ, Черствый ЕД. Экспрессия подокаликсина в клубочках почки при нефротическом синдроме у детей. Здравоохранение (Минск) 2011; (3): 4-8</mixed-citation><mixed-citation xml:lang="en">Sakharov IV, SukaloAV, Tcherstvij ED.Ekspressija podokaliksina v klubochkakh pochki pri nefroticheskom syndrome u detej. Zdravookhranenie (Minsk) 2011; (3): 4-8 (In Russ).</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Haraldsson B, Nystrom J, Deen WM. Properties of the glomerular barrier and mechanisms of proteinuria. Physiol Rev 2008; 88 (2): 451-487. Doi:10.1152/physrev.00055.2006</mixed-citation><mixed-citation xml:lang="en">Haraldsson B, Nystrom J, Deen WM. Properties of the glomerular barrier and mechanisms of proteinuria. Physiol Rev 2008; 88 (2): 451-487. Doi:10.1152/physrev.00055.2006</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Scott RP, Quaggin SE. The cell biology of renal filtration. J Cell Biol 2015; 209 (2): 199-210. Doi: 10.1083/jcb.201410017</mixed-citation><mixed-citation xml:lang="en">Scott RP, Quaggin SE. The cell biology of renal filtration. J Cell Biol 2015; 209 (2): 199-210. Doi: 10.1083/jcb.201410017</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Петросян ЭК. Подоцит: строение и роль в развитии нефротического синдрома. Нефрология и диализ 2006; 8 (2): 112121</mixed-citation><mixed-citation xml:lang="en">Petrosyan EK. Podotsit: stroenie i rol v razvitii inefroticheskogo syndroma. Nefrologija i dializ 2006; 8 (2): 112-121 (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Грене ГЙ, Кисс Е. Нефротический синдром: гистопатологическая дифференциальная диагностика. Часть 1: определение, классификация, патофизиология, генетические формы. Нефрология 2007; 11(2): 88-93</mixed-citation><mixed-citation xml:lang="en">Grene GI, KissE. Nefroticheskij syndrom: gistopatologicheskaja differentsial'naja diagnostika. Chast 1: opredelenie, klassifikatsija, patofisiologija, geneticheskie formy. Nefrologija 2007; 11 (2): 88-93 (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Серов ВВ. Функциональная морфология почек. В: Тареева ИЕ, ред. Нефрология. Руководство для врачей. Медицина, М., 2000; 145-150 [Serov VV. Funrtsional’naja morfologija pochek.V: Tareeva IE, red. Nefrologija. Rukovodstvo dlya vrachej. Meditsina, M., 2000; 145-150 (In Russ.)]</mixed-citation><mixed-citation xml:lang="en">Serov VV. Funrtsional’naja morfologija pochek.V: Tareeva IE, red. Nefrologija. Rukovodstvo dlya vrachej. Meditsina, M., 2000; 145-150 (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Rostgaard J, Qvortrup K. Sieve plugs in fenestrae of glomerular capillaries-site of filtration barrier? Cell Tissues Organs (Print) 2002; 170: 132-138. Doi: 10.1159/000046186</mixed-citation><mixed-citation xml:lang="en">Rostgaard J, Qvortrup K. Sieve plugs in fenestrae of glomerular capillaries-site of filtration barrier? Cell Tissues Organs (Print) 2002; 170: 132-138. Doi: 10.1159/000046186</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Deen WM. What determines glomerular capillary permeability? J Clin Invest 2004; 114 (10): 1412-1414. Doi: 10.1172/JCI23577</mixed-citation><mixed-citation xml:lang="en">Deen WM. What determines glomerular capillary permeability? J Clin Invest 2004; 114 (10): 1412-1414. Doi: 10.1172/JCI23577</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Jeansson M, Haraldsson B. Morphological and functional evidence for an important role of the endothelial cell glycocalyx in the glomerular barrier. Am J Physiol Renal Physiol 2006; 290: F111-F116. Doi: 10.1152/ajprenal.00173.2005</mixed-citation><mixed-citation xml:lang="en">Jeansson M, Haraldsson B. Morphological and functional evidence for an important role of the endothelial cell glycocalyx in the glomerular barrier. Am J Physiol Renal Physiol 2006; 290: F111-F116. Doi: 10.1152/ajprenal.00173.2005</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Curry FE, Adamson RH. Endothelial glycocalyx: permeability barrier and mechanosensor. Ann Biomed Eng 2012; 40: 828-839. Doi: 10.1007/s10439-011-0429-8</mixed-citation><mixed-citation xml:lang="en">Curry FE, Adamson RH. Endothelial glycocalyx: permeability barrier and mechanosensor. Ann Biomed Eng 2012; 40: 828-839. Doi: 10.1007/s10439-011-0429-8</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Lennon R, Byron A, Humphries JD et al. Global analysis reveals the complexity of the human glomerular extracellular matrix. J Am Soc Nephrol 2014; 25: 939-951. Doi: 10.1681/ASN.2013030233</mixed-citation><mixed-citation xml:lang="en">Lennon R, Byron A, Humphries JD et al. Global analysis reveals the complexity of the human glomerular extracellular matrix. J Am Soc Nephrol 2014; 25: 939-951. Doi: 10.1681/ASN.2013030233</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Мельник АА. Фокально-сегментарный гломерулоскле-роз: генетический анализ и целевая терапия. Pocki 2018; 7 (1): 35-49. Doi: 10.22141/2307-1257.7.1.2018.122218</mixed-citation><mixed-citation xml:lang="en">Mel’nik AA. Fokal’no-segmentarniy glomeruloskleroz: geneticheskij analiz i tselevaja terapiya (In Russ). Doi: 10.22141/2307-1257.7.1.2018.122218</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Lowik MM, Groenen PJ, Levtchenko EN et al. Molecular genetic analysis of podocyte genes in focal segmental glomerulosclerosis - a review. Eur J Pediatr 2009; 168: 1291-1304. Doi: 10.1007/s00431-009-1017-x</mixed-citation><mixed-citation xml:lang="en">Lowik MM, Groenen PJ, Levtchenko EN et al. Molecular genetic analysis of podocyte genes in focal segmental glomerulosclerosis - a review. Eur J Pediatr 2009; 168: 1291-1304. Doi: 10.1007/s00431-009-1017-x</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Neal CR, Muston PR, Njegovan D et al. Glomerular filtration into the subpodocyte space is highly restricted under physiological perfusion conditions. Am J Physiol Renal Physiol 2007; 293 (6): F1787-F1798. Doi: 10.1152/ajprenal.00157.2007</mixed-citation><mixed-citation xml:lang="en">Neal CR, Muston PR, Njegovan D et al. Glomerular filtration into the subpodocyte space is highly restricted under physiological perfusion conditions. Am J Physiol Renal Physiol 2007; 293 (6): F1787-F1798. Doi: 10.1152/ajprenal.00157.2007</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Akchurin O, Reidy KJ. Genetic causes of proteinuria and nephritic syndrome: Impact on podocyte pathobiology. Pediatr Nephrol 2014, Published online: 02 March 2014. Doi: 10.1007/s00467-014-2753-3</mixed-citation><mixed-citation xml:lang="en">Akchurin O, Reidy KJ. Genetic causes of proteinuria and nephritic syndrome: Impact on podocyte pathobiology. Pediatr Nephrol 2014, Published online: 02 March 2014. Doi: 10.1007/s00467-014-2753-3</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Жангожин ЕЖ. Генетически-детерминированные формы фокально-сегментарного гломерулосклероза. Медицина и экология 2016; (1): 24-31</mixed-citation><mixed-citation xml:lang="en">Zhangozhin EZh. Geneticheski-determinirovannye formy fokal’no-segmentarnogo glomeruloskleroza. Meditsina i ekologija 2016; (1): 24-31 (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">D’Agati V. Pathologic classification of focal segmental glomerulosclerosis. Sem Nephrol 2003; 23 (2): 117-134. Doi: 10.1053/snep.2003.50012</mixed-citation><mixed-citation xml:lang="en">D’Agati V. Pathologic classification of focal segmental glomerulosclerosis. Sem Nephrol 2003; 23 (2): 117-134. Doi: 10.1053/snep.2003.50012</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Бобкова ИН, Козловская ЛВ, Цыгин АН, Шилов ЕМ. Клинические рекомендации по диагностике и лечению фокально-сегментарного гломерулосклероза. Нефрология 2015; 19 (1): 78-85.</mixed-citation><mixed-citation xml:lang="en">Bobkova IN, Kozlovskaya LV, Tsygin AN, Shilov EM. Clinical practice guideline for diagnostics and treatment of focal segmental glomerulosclerosis. Nefrologija 2015; 19 (1): 78-85. (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">D’Agati VD, Fogo AB, Bruijn JA, Jennette JC. Pathologic classification of focal segmental glomerulosclerosis: a new working proposal. Am J Kidney Dis 2004; 43 (2): 368-382</mixed-citation><mixed-citation xml:lang="en">D’Agati VD, Fogo AB, Bruijn JA, Jennette JC. Pathologic classification of focal segmental glomerulosclerosis: a new working proposal. Am J Kidney Dis 2004; 43 (2): 368-382</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Stroes ES, Joles JA, Chang PC et al. Impaired endothelial function in patients with nephrotic range proteinuria. Kidney Int 1995; 48 (2): 544-550</mixed-citation><mixed-citation xml:lang="en">Stroes ES, Joles JA, Chang PC et al. Impaired endothelial function in patients with nephrotic range proteinuria. Kidney Int 1995; 48 (2): 544-550</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Sarin H. Physiologic upper limits of pore size of different blood capillary types and another prospective on the dual pore theory of microvascular permeability. J Angiogenes Res 2010; 2: 14. Doi: 10.1186/2040-2384-2-14</mixed-citation><mixed-citation xml:lang="en">Sarin H. Physiologic upper limits of pore size of different blood capillary types and another prospective on the dual pore theory of microvascular permeability. J Angiogenes Res 2010; 2: 14. Doi: 10.1186/2040-2384-2-14</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Satchell SC, Braet F. Glomerular endothelial cell fenestrations: an integral component of the glomerular filtration barrier. Am J Physiol Renal Physiol 2009; 296 (5): F947-F956. Doi: 10.1152/ajprenal.90601.2008</mixed-citation><mixed-citation xml:lang="en">Satchell SC, Braet F. Glomerular endothelial cell fenestrations: an integral component of the glomerular filtration barrier. Am J Physiol Renal Physiol 2009; 296 (5): F947-F956. Doi: 10.1152/ajprenal.90601.2008</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Reitsma S, Slaaf DW, Vink Het al. The endothelial glycocalyx: composition, functions, and visualization. Pflugers Arch 2007; 454 (3): 345-359. Doi: 10.1007/s00424-007-0212-8</mixed-citation><mixed-citation xml:lang="en">Reitsma S, Slaaf DW, Vink Het al. The endothelial glycocalyx: composition, functions, and visualization. Pflugers Arch 2007; 454 (3): 345-359. Doi: 10.1007/s00424-007-0212-8</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Garsen M, Rops AZWMM, Rabelink TJ et al. The role of heparanase and the endothelial glycocalyx in the development of proteinuria. Nephrol Dial Transplant 2014; 29: 49-55. Doi: 10.1093/ndt/gfth10</mixed-citation><mixed-citation xml:lang="en">Garsen M, Rops AZWMM, Rabelink TJ et al. The role of heparanase and the endothelial glycocalyx in the development of proteinuria. Nephrol Dial Transplant 2014; 29: 49-55. Doi: 10.1093/ndt/gfth10</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Hjalmarsson C, Johansson BR, Haraldsson B. Electron microscopic evaluation of the endothelial surface layer of glomerular capillaries. Microvasc Res 2004; 67: 9-17. Doi: 10.1016/j.mvr.2003.10.001</mixed-citation><mixed-citation xml:lang="en">Hjalmarsson C, Johansson BR, Haraldsson B. Electron microscopic evaluation of the endothelial surface layer of glomerular capillaries. Microvasc Res 2004; 67: 9-17. Doi: 10.1016/j.mvr.2003.10.001</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Andersson M, Nilsson U, Hjalmarsson C et al. Mild renal ischemia-reperfusion reduces charge and size selectivity of the glomerular barrier. Am J Physiol Renal Physiol 2007; 292: F1802-F1809. Doi: 10.1152/ajprenal.00152.2006</mixed-citation><mixed-citation xml:lang="en">Andersson M, Nilsson U, Hjalmarsson C et al. Mild renal ischemia-reperfusion reduces charge and size selectivity of the glomerular barrier. Am J Physiol Renal Physiol 2007; 292: F1802-F1809. Doi: 10.1152/ajprenal.00152.2006</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Galvis-Ramirez MF, Quintana-Castillo JC, Bueno-Sanchez JC. Novel insights into the role of glycans in the pathophysiology of glomerular endotheliosis in preeclampsia. Front Physiol 2018; 9: Article 1470. 10.3389/fphys.2018.01470</mixed-citation><mixed-citation xml:lang="en">Galvis-Ramirez MF, Quintana-Castillo JC, Bueno-Sanchez JC. Novel insights into the role of glycans in the pathophysiology of glomerular endotheliosis in preeclampsia. Front Physiol 2018; 9: Article 1470. 10.3389/fphys.2018.01470</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Gelberg H, Healy L, Whiteley H et al. In vivo enzymatic removal of alpha 2--&gt;6-linked sialic acid from the glomerular filtration barrier results in podocyte charge alteration and glomerular injury. Lab Invest 1996; 74 (5): 907-920</mixed-citation><mixed-citation xml:lang="en">Gelberg H, Healy L, Whiteley H et al. In vivo enzymatic removal of alpha 2--&gt;6-linked sialic acid from the glomerular filtration barrier results in podocyte charge alteration and glomerular injury. Lab Invest 1996; 74 (5): 907-920</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Jeansson M, Haraldsson B. Glomerular size and charge selectivity in the mouse after exposure to glucosaminoglycan-degrading enzymes. Am Soc Nephrol 2003; 14 (7): 1756-1765</mixed-citation><mixed-citation xml:lang="en">Jeansson M, Haraldsson B. Glomerular size and charge selectivity in the mouse after exposure to glucosaminoglycan-degrading enzymes. Am Soc Nephrol 2003; 14 (7): 1756-1765</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Meuwese MC, Broekhuizen LN, Kuikhoven M et al. Endothelial surface layer degradation by chronic hyaluronidase infusion induces proteinuria in apolipoprotein E-deficient mice. PLoS One 2010; 5 (12): e14262. Doi: 10.1371/journal.pone.0014262</mixed-citation><mixed-citation xml:lang="en">Meuwese MC, Broekhuizen LN, Kuikhoven M et al. Endothelial surface layer degradation by chronic hyaluronidase infusion induces proteinuria in apolipoprotein E-deficient mice. PLoS One 2010; 5 (12): e14262. Doi: 10.1371/journal.pone.0014262</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Dane MJ, van den Berg BM, Avramut MC et al.Glomerular endothelial surface layer acts as a barrier against albumin filtration. Am J Pathol 2013; 182 (5): 1532-1540. Doi: 10.1016/j.ajpath.2013.01.049</mixed-citation><mixed-citation xml:lang="en">Dane MJ, van den Berg BM, Avramut MC et al.Glomerular endothelial surface layer acts as a barrier against albumin filtration. Am J Pathol 2013; 182 (5): 1532-1540. Doi: 10.1016/j.ajpath.2013.01.049</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Jeansson B, Bjorck K, Tenstad O, Haraldsson B. Adriamy-cin alters glomerular endothelium to induce proteinuria. J Am Soc Nephrol 2009; 20: 114-122. Doi: 10.1681/ASN.2007111205</mixed-citation><mixed-citation xml:lang="en">Jeansson B, Bjorck K, Tenstad O, Haraldsson B. Adriamy-cin alters glomerular endothelium to induce proteinuria. J Am Soc Nephrol 2009; 20: 114-122. Doi: 10.1681/ASN.2007111205</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Friden V, Oveland E, Tenstad o et al. The glomerular endothelial cell coat is essential for glomerular filtration. Kidney Int 2011; 79 (12): 1322-1330. Doi: 10.1038/ki.2011.58</mixed-citation><mixed-citation xml:lang="en">Friden V, Oveland E, Tenstad o et al. The glomerular endothelial cell coat is essential for glomerular filtration. Kidney Int 2011; 79 (12): 1322-1330. Doi: 10.1038/ki.2011.58</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Salmon AH, Ferguson JK, Burford JL et al. Loss of the endothelial glycocalyx links albuminuria and vascular dysfunction. J Am Soc Nephrol 2012; 23: 1339-1350. Doi: 10.1681/ASN.2012010017</mixed-citation><mixed-citation xml:lang="en">Salmon AH, Ferguson JK, Burford JL et al. Loss of the endothelial glycocalyx links albuminuria and vascular dysfunction. J Am Soc Nephrol 2012; 23: 1339-1350. Doi: 10.1681/ASN.2012010017</mixed-citation></citation-alternatives></ref><ref id="cit36"><label>36</label><citation-alternatives><mixed-citation xml:lang="ru">Salmon AH, Satchall SC. Endothelial glycocalyx dysfunction in disease: albuminuria and increased microvascular permeability. J Pathol 2012; 226 (4): 562-574. Doi: 10.1002/path.3964</mixed-citation><mixed-citation xml:lang="en">Salmon AH, Satchall SC. Endothelial glycocalyx dysfunction in disease: albuminuria and increased microvascular permeability. J Pathol 2012; 226 (4): 562-574. Doi: 10.1002/path.3964</mixed-citation></citation-alternatives></ref><ref id="cit37"><label>37</label><citation-alternatives><mixed-citation xml:lang="ru">Kuwabara A, Satoh M, Tomita N et al. Deterioration of glomerular endothelial surface layer induced by oxidative stress is implicated in altered permeability of macromolecules in Zucker fatty rats. Diabetologia 2010; 53 (9): 2056-2065. Doi: 10.1007/s00125-010-1810-0</mixed-citation><mixed-citation xml:lang="en">Kuwabara A, Satoh M, Tomita N et al. Deterioration of glomerular endothelial surface layer induced by oxidative stress is implicated in altered permeability of macromolecules in Zucker fatty rats. Diabetologia 2010; 53 (9): 2056-2065. Doi: 10.1007/s00125-010-1810-0</mixed-citation></citation-alternatives></ref><ref id="cit38"><label>38</label><citation-alternatives><mixed-citation xml:lang="ru">Haraldsson B, Nystrom J. The glomerular endothelium: new insights on function and structure. Curr Opin Nephrol Hypertens 2012; 21 (3): 258-263. Doi: 10.1097/MNH.0b013e3283522e7a</mixed-citation><mixed-citation xml:lang="en">Haraldsson B, Nystrom J. The glomerular endothelium: new insights on function and structure. Curr Opin Nephrol Hypertens 2012; 21 (3): 258-263. Doi: 10.1097/MNH.0b013e3283522e7a</mixed-citation></citation-alternatives></ref><ref id="cit39"><label>39</label><citation-alternatives><mixed-citation xml:lang="ru">Nieuwdorp M, Mooij HL, Kroon J et al. Endothelial glycocalyx damage coincides with microalbuminuria in type 1 diabetes. Diabetes 2006; 55 (4): 1127-1132</mixed-citation><mixed-citation xml:lang="en">Nieuwdorp M, Mooij HL, Kroon J et al. Endothelial glycocalyx damage coincides with microalbuminuria in type 1 diabetes. Diabetes 2006; 55 (4): 1127-1132</mixed-citation></citation-alternatives></ref><ref id="cit40"><label>40</label><citation-alternatives><mixed-citation xml:lang="ru">Broekhuizen LN, Lemkes BA, Mooij HL et al. Effect of superoxide on endothelial glycocalix and vascular permeability in patients with type 2 diabetes mellitus. Diabetologia 2010; 53 (12): 2646-2655. Doi: 10.1007/s00125-010-1910-x</mixed-citation><mixed-citation xml:lang="en">Broekhuizen LN, Lemkes BA, Mooij HL et al. Effect of superoxide on endothelial glycocalix and vascular permeability in patients with type 2 diabetes mellitus. Diabetologia 2010; 53 (12): 2646-2655. Doi: 10.1007/s00125-010-1910-x</mixed-citation></citation-alternatives></ref><ref id="cit41"><label>41</label><citation-alternatives><mixed-citation xml:lang="ru">Singh A, Friden V, Dasgupta I et al. High glucose causes dysfunction of the human glomerular endothelial glycocalyx. Am J Physiol Renal Physiol 2011; 300 (1): F40-F48. Doi: 10.1152/ajpre-nal.00103.2010</mixed-citation><mixed-citation xml:lang="en">Singh A, Friden V, Dasgupta I et al. High glucose causes dysfunction of the human glomerular endothelial glycocalyx. Am J Physiol Renal Physiol 2011; 300 (1): F40-F48. Doi: 10.1152/ajpre-nal.00103.2010</mixed-citation></citation-alternatives></ref><ref id="cit42"><label>42</label><citation-alternatives><mixed-citation xml:lang="ru">Toyoda M, Najafian B, Kim Y et al. Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy. Diabetes 2007; 56 (8): 2155-2160. Doi: 10.2337/db07-0019</mixed-citation><mixed-citation xml:lang="en">Toyoda M, Najafian B, Kim Y et al. Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy. Diabetes 2007; 56 (8): 2155-2160. Doi: 10.2337/db07-0019</mixed-citation></citation-alternatives></ref><ref id="cit43"><label>43</label><citation-alternatives><mixed-citation xml:lang="ru">Persson F, Rossing P, Hoving P et al. Endothelial dysfunction and inflammation predict development of diabetic nephropathy in the irbesartan in patients with type 2 diabetes and microalbuminuria (IRMA2) study. Scand J Clin Lab Invest 2008; 68 (8): 731-738. Doi: 10.1080/00365510802187226</mixed-citation><mixed-citation xml:lang="en">Persson F, Rossing P, Hoving P et al. Endothelial dysfunction and inflammation predict development of diabetic nephropathy in the irbesartan in patients with type 2 diabetes and microalbuminuria (IRMA2) study. Scand J Clin Lab Invest 2008; 68 (8): 731-738. Doi: 10.1080/00365510802187226</mixed-citation></citation-alternatives></ref><ref id="cit44"><label>44</label><citation-alternatives><mixed-citation xml:lang="ru">Daehn LS. Glomerular endothelial cell stress and cross-talk with podocyte in early diabetic kidney disease. Front Med 2018; 5: Article 76, published 23 March 2018. Doi: 10.3389/fmed.2018.00076</mixed-citation><mixed-citation xml:lang="en">Daehn LS. Glomerular endothelial cell stress and cross-talk with podocyte in early diabetic kidney disease. Front Med 2018; 5: Article 76, published 23 March 2018. Doi: 10.3389/fmed.2018.00076</mixed-citation></citation-alternatives></ref><ref id="cit45"><label>45</label><citation-alternatives><mixed-citation xml:lang="ru">Ogino S. An electron microscopic study of the glomerular alterations of pure-preeclampsia. Nihon Jinzo Gakkai Shi 1999; 41(4): 413-429</mixed-citation><mixed-citation xml:lang="en">Ogino S. An electron microscopic study of the glomerular alterations of pure-preeclampsia. Nihon Jinzo Gakkai Shi 1999; 41(4): 413-429</mixed-citation></citation-alternatives></ref><ref id="cit46"><label>46</label><citation-alternatives><mixed-citation xml:lang="ru">Levine RJ, Maynard SE, Qian C et al. Circulating angiogenic factors and the risk of preeclampsia. N Engl J Med 2004; 350 (7): 672-683. Doi: 10.1056/NEJMoa031884</mixed-citation><mixed-citation xml:lang="en">Levine RJ, Maynard SE, Qian C et al. Circulating angiogenic factors and the risk of preeclampsia. N Engl J Med 2004; 350 (7): 672-683. Doi: 10.1056/NEJMoa031884</mixed-citation></citation-alternatives></ref><ref id="cit47"><label>47</label><citation-alternatives><mixed-citation xml:lang="ru">Karumanchi SA, Maynard SE, Stillman IE et al. Preeclampsia: a renal perspective. Kidney Int 2005; 67 (6): 2101-2113. Doi: 10.1111/j.1523-1755.2005.00316.x</mixed-citation><mixed-citation xml:lang="en">Karumanchi SA, Maynard SE, Stillman IE et al. Preeclampsia: a renal perspective. Kidney Int 2005; 67 (6): 2101-2113. Doi: 10.1111/j.1523-1755.2005.00316.x</mixed-citation></citation-alternatives></ref><ref id="cit48"><label>48</label><citation-alternatives><mixed-citation xml:lang="ru">Maynard SE, Venkatesha S, Thadhani R, Karumanchi SA. Soluble Fms-like tyrosine kinase 1 and endothelial dysfunction in the pathogenesis of preeclampsia. Pediatr Res 2005; 57 (5 Pt2): 1R-7R. Doi: 10.1203/01.PDR.0000159567.85157.B7</mixed-citation><mixed-citation xml:lang="en">Maynard SE, Venkatesha S, Thadhani R, Karumanchi SA. Soluble Fms-like tyrosine kinase 1 and endothelial dysfunction in the pathogenesis of preeclampsia. Pediatr Res 2005; 57 (5 Pt2): 1R-7R. Doi: 10.1203/01.PDR.0000159567.85157.B7</mixed-citation></citation-alternatives></ref><ref id="cit49"><label>49</label><citation-alternatives><mixed-citation xml:lang="ru">Levine RJ, Lam C, Qian C et al. Soluble endoglin and other circulating antiangiogenic factors in preeclampsia. N Engl J Med 2006; 355 (10): 992-1005. Doi: 10.1056/NEJMoa055352</mixed-citation><mixed-citation xml:lang="en">Levine RJ, Lam C, Qian C et al. Soluble endoglin and other circulating antiangiogenic factors in preeclampsia. N Engl J Med 2006; 355 (10): 992-1005. Doi: 10.1056/NEJMoa055352</mixed-citation></citation-alternatives></ref><ref id="cit50"><label>50</label><citation-alternatives><mixed-citation xml:lang="ru">Moran P, Baylis PH, Lindhelma MD, Davison JM. Glomerular ultrafiltration in normal and preeclamptic pregnancy. J Am Soc Nephrol 2003; 14: 648-652. Doi: 10.1097/01ASN0000051724.66235.E0</mixed-citation><mixed-citation xml:lang="en">Moran P, Baylis PH, Lindhelma MD, Davison JM. Glomerular ultrafiltration in normal and preeclamptic pregnancy. J Am Soc Nephrol 2003; 14: 648-652. Doi: 10.1097/01ASN0000051724.66235.E0</mixed-citation></citation-alternatives></ref><ref id="cit51"><label>51</label><citation-alternatives><mixed-citation xml:lang="ru">Lafayette RA, Druzin M, Sibley R et al. Nature of glomerular dysfunction in pre-eclampsia. Kidney Int 1998; 54 (4): 1240-1249. Doi: 10.1046/j.1523-1755.1998.00097.x</mixed-citation><mixed-citation xml:lang="en">Lafayette RA, Druzin M, Sibley R et al. Nature of glomerular dysfunction in pre-eclampsia. Kidney Int 1998; 54 (4): 1240-1249. Doi: 10.1046/j.1523-1755.1998.00097.x</mixed-citation></citation-alternatives></ref><ref id="cit52"><label>52</label><citation-alternatives><mixed-citation xml:lang="ru">Strevens H, Wide-Swensson D, Hansen A et al. Glomerular endotheliosis in normal pregnancy and pre-eclampsia. BJOG 2003; 110: 831-836. Doi: 10.1111/j.1471-0528.2003.02162.x</mixed-citation><mixed-citation xml:lang="en">Strevens H, Wide-Swensson D, Hansen A et al. Glomerular endotheliosis in normal pregnancy and pre-eclampsia. BJOG 2003; 110: 831-836. Doi: 10.1111/j.1471-0528.2003.02162.x</mixed-citation></citation-alternatives></ref><ref id="cit53"><label>53</label><citation-alternatives><mixed-citation xml:lang="ru">Naicker T, Randeree IG, Moodley J et al. Correlation between histological changes and loss of anionic charge of the glomerular basement membrane in early-onset pre-eclampsia. Nephron 1997; 75: 201-207. Doi: 10.1159/000189532</mixed-citation><mixed-citation xml:lang="en">Naicker T, Randeree IG, Moodley J et al. Correlation between histological changes and loss of anionic charge of the glomerular basement membrane in early-onset pre-eclampsia. Nephron 1997; 75: 201-207. Doi: 10.1159/000189532</mixed-citation></citation-alternatives></ref><ref id="cit54"><label>54</label><citation-alternatives><mixed-citation xml:lang="ru">Taneda S, Honda K, Ohno M et al. Podocyte and endothelial injury in focal segmental glomerulosclerosis: an ultrastructural analysis. Virchows Arch 2015; 467: 449-458. Doi: 10.1007/s00428-015-1821-9</mixed-citation><mixed-citation xml:lang="en">Taneda S, Honda K, Ohno M et al. Podocyte and endothelial injury in focal segmental glomerulosclerosis: an ultrastructural analysis. Virchows Arch 2015; 467: 449-458. Doi: 10.1007/s00428-015-1821-9</mixed-citation></citation-alternatives></ref><ref id="cit55"><label>55</label><citation-alternatives><mixed-citation xml:lang="ru">Leontsini M. Mesangiolysis. HIPPOKRATIA 2003; 7: 147-151</mixed-citation><mixed-citation xml:lang="en">Leontsini M. Mesangiolysis. HIPPOKRATIA 2003; 7: 147-151</mixed-citation></citation-alternatives></ref><ref id="cit56"><label>56</label><citation-alternatives><mixed-citation xml:lang="ru">Futrakul N, Butthep P, Futrakul P. Biomarkers of endothelial injury in local segmental glomerulosclerotic nephrosis. Ren Fail2005; 27 (4): 393-395</mixed-citation><mixed-citation xml:lang="en">Futrakul N, Butthep P, Futrakul P. Biomarkers of endothelial injury in local segmental glomerulosclerotic nephrosis. Ren Fail2005; 27 (4): 393-395</mixed-citation></citation-alternatives></ref><ref id="cit57"><label>57</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang Q, Zeng C, Fu Y et al. Biomarkers of endothelial dysfunction in patients with primary focal segmental glomerulosclerosis. Nephrology (Carlton) 2012; 17 (4): 338-345. Doi: 10.1111/j.1440-1797.2012.o1575.x</mixed-citation><mixed-citation xml:lang="en">Zhang Q, Zeng C, Fu Y et al. Biomarkers of endothelial dysfunction in patients with primary focal segmental glomerulosclerosis. Nephrology (Carlton) 2012; 17 (4): 338-345. Doi: 10.1111/j.1440-1797.2012.o1575.x</mixed-citation></citation-alternatives></ref><ref id="cit58"><label>58</label><citation-alternatives><mixed-citation xml:lang="ru">Tkaczyk M, Czupryniak A, Owczaker D et al. Markers of endothelial dysfunction in children with idiopathic nephrotic syndrome. Am J Nephrol 2008; 28 (2): 197-202. Doi: 10.1159/000110088</mixed-citation><mixed-citation xml:lang="en">Tkaczyk M, Czupryniak A, Owczaker D et al. Markers of endothelial dysfunction in children with idiopathic nephrotic syndrome. Am J Nephrol 2008; 28 (2): 197-202. Doi: 10.1159/000110088</mixed-citation></citation-alternatives></ref><ref id="cit59"><label>59</label><citation-alternatives><mixed-citation xml:lang="ru">Shouman M, Abdallah N, Tablawy El N, Rashed L. chemical markers of endothelial dysfunction in pediatric nephrotic syndrome. Arch MedSci 2009; 5: 415-421</mixed-citation><mixed-citation xml:lang="en">Shouman M, Abdallah N, Tablawy El N, Rashed L. chemical markers of endothelial dysfunction in pediatric nephrotic syndrome. Arch MedSci 2009; 5: 415-421</mixed-citation></citation-alternatives></ref><ref id="cit60"><label>60</label><citation-alternatives><mixed-citation xml:lang="ru">Kitamura H, Shimizu A, MasudaYet al. Apoptosis in glomerular endothelial cells during the development of glomerulosclerosis in the remnant-kidney model. Exp Nephrol 1998; 6 (4): 328-336</mixed-citation><mixed-citation xml:lang="en">Kitamura H, Shimizu A, MasudaYet al. Apoptosis in glomerular endothelial cells during the development of glomerulosclerosis in the remnant-kidney model. Exp Nephrol 1998; 6 (4): 328-336</mixed-citation></citation-alternatives></ref><ref id="cit61"><label>61</label><citation-alternatives><mixed-citation xml:lang="ru">Song YR, You SJ, LeeYM et al. Activation of hypoxia-inducible factor attenuates renal injury in rat remnant kidney. Nephrol Dial Transplant 2010; 25 (1): 77-85. Doi: 10.1093/ndt/gfp454</mixed-citation><mixed-citation xml:lang="en">Song YR, You SJ, LeeYM et al. Activation of hypoxia-inducible factor attenuates renal injury in rat remnant kidney. Nephrol Dial Transplant 2010; 25 (1): 77-85. Doi: 10.1093/ndt/gfp454</mixed-citation></citation-alternatives></ref><ref id="cit62"><label>62</label><citation-alternatives><mixed-citation xml:lang="ru">Daehn I, Casalena G, Zhang T et al. Endothelial mitochondrial oxidative stress determines podocyte depletion in segmental glomerulosclerosis. J Clin Invest 2014; 124 (4): 1608-1621. Doi: 10.1172/JCI71195</mixed-citation><mixed-citation xml:lang="en">Daehn I, Casalena G, Zhang T et al. Endothelial mitochondrial oxidative stress determines podocyte depletion in segmental glomerulosclerosis. J Clin Invest 2014; 124 (4): 1608-1621. Doi: 10.1172/JCI71195</mixed-citation></citation-alternatives></ref><ref id="cit63"><label>63</label><citation-alternatives><mixed-citation xml:lang="ru">van den Hoven MJ, Rops AL, Vlodavsky I et al. Heparanase in glomerular diseases. KidneyInt 2007; 72 (5): 543-548. Doi: 10.1038/sj.ki.5002337</mixed-citation><mixed-citation xml:lang="en">van den Hoven MJ, Rops AL, Vlodavsky I et al. Heparanase in glomerular diseases. KidneyInt 2007; 72 (5): 543-548. Doi: 10.1038/sj.ki.5002337</mixed-citation></citation-alternatives></ref><ref id="cit64"><label>64</label><citation-alternatives><mixed-citation xml:lang="ru">Borza DB. Glomerular basement membrane heparan sulfate in health and disease: a regulator of local complement activation. Matrix Biol 2017; 57-58: 299-310. Doi: 10.1016/j.matbio.2016.09.002</mixed-citation><mixed-citation xml:lang="en">Borza DB. Glomerular basement membrane heparan sulfate in health and disease: a regulator of local complement activation. Matrix Biol 2017; 57-58: 299-310. Doi: 10.1016/j.matbio.2016.09.002</mixed-citation></citation-alternatives></ref><ref id="cit65"><label>65</label><citation-alternatives><mixed-citation xml:lang="ru">Goldsmidt O, Zcharia E, Cohen M et al. Heparanase mediates cell adhesion independent of its enzymatic activity. FASEB J 2003; 17 (9): 1015-1025. Doi: 10.1096/fj.02-0773com</mixed-citation><mixed-citation xml:lang="en">Goldsmidt O, Zcharia E, Cohen M et al. Heparanase mediates cell adhesion independent of its enzymatic activity. FASEB J 2003; 17 (9): 1015-1025. Doi: 10.1096/fj.02-0773com</mixed-citation></citation-alternatives></ref><ref id="cit66"><label>66</label><citation-alternatives><mixed-citation xml:lang="ru">Levidiotis V, Kanellis J, Ierino FL et al. Increased expression of heparanase in puromycin aminonucleoside nephrosis. Kidney Int 2001; 60 (4): 1287-1296. Doi: 10.1046/j.1523-1755.2001.00934.x</mixed-citation><mixed-citation xml:lang="en">Levidiotis V, Kanellis J, Ierino FL et al. Increased expression of heparanase in puromycin aminonucleoside nephrosis. Kidney Int 2001; 60 (4): 1287-1296. Doi: 10.1046/j.1523-1755.2001.00934.x</mixed-citation></citation-alternatives></ref><ref id="cit67"><label>67</label><citation-alternatives><mixed-citation xml:lang="ru">van Bruggen MC, Kramers K, Hylkema MN et al. Decrease of heparan sulfate staining in the glomerular basement membrane in murine lupus nephritis. Am J Pathol 1995; 146 (3): 753-763</mixed-citation><mixed-citation xml:lang="en">van Bruggen MC, Kramers K, Hylkema MN et al. Decrease of heparan sulfate staining in the glomerular basement membrane in murine lupus nephritis. Am J Pathol 1995; 146 (3): 753-763</mixed-citation></citation-alternatives></ref><ref id="cit68"><label>68</label><citation-alternatives><mixed-citation xml:lang="ru">Levidiotis V, Freeman C, Tikellis C et al. Heparanase is involved in the pathogenesis of proteinuria as a result of glomerulonephritis. J Am Soc Nephrol 2004; 15 (1): 68-78. Doi: 10.1097/01.ASN.0000103229.25389.40</mixed-citation><mixed-citation xml:lang="en">Levidiotis V, Freeman C, Tikellis C et al. Heparanase is involved in the pathogenesis of proteinuria as a result of glomerulonephritis. J Am Soc Nephrol 2004; 15 (1): 68-78. Doi: 10.1097/01.ASN.0000103229.25389.40</mixed-citation></citation-alternatives></ref><ref id="cit69"><label>69</label><citation-alternatives><mixed-citation xml:lang="ru">Kramer A, van den Hoven M, Rops A et al. Induction of glomerular heparanase expression in rats with adriamycin nephropathy is regulated by reactive oxygen species and the renin-angiotensin system. J Am Soc Nephrol 2006; 17 (9): 2513-2520. Doi: 10.1681/ASN.2006020184</mixed-citation><mixed-citation xml:lang="en">Kramer A, van den Hoven M, Rops A et al. Induction of glomerular heparanase expression in rats with adriamycin nephropathy is regulated by reactive oxygen species and the renin-angiotensin system. J Am Soc Nephrol 2006; 17 (9): 2513-2520. Doi: 10.1681/ASN.2006020184</mixed-citation></citation-alternatives></ref><ref id="cit70"><label>70</label><citation-alternatives><mixed-citation xml:lang="ru">van den Hoven MJ, Rops AL, Bakker MA et al. Increased expression of heparanase in overt diabetic nephropathy. Kidney Int 2006; 79 (12): 2100-2108. Doi: 10.1038/sj.ki.5001985</mixed-citation><mixed-citation xml:lang="en">van den Hoven MJ, Rops AL, Bakker MA et al. Increased expression of heparanase in overt diabetic nephropathy. Kidney Int 2006; 79 (12): 2100-2108. Doi: 10.1038/sj.ki.5001985</mixed-citation></citation-alternatives></ref><ref id="cit71"><label>71</label><citation-alternatives><mixed-citation xml:lang="ru">Rops AL, van den Hoven MJ, Bakker MA et al. Expression of glomerular heparan sulphate domains in murine and human lupus nephritis. Nephrol Dial Transplant 2007; 22 (7): 1891-1902. Doi: 10.1093/ndt/gfm194</mixed-citation><mixed-citation xml:lang="en">Rops AL, van den Hoven MJ, Bakker MA et al. Expression of glomerular heparan sulphate domains in murine and human lupus nephritis. Nephrol Dial Transplant 2007; 22 (7): 1891-1902. Doi: 10.1093/ndt/gfm194</mixed-citation></citation-alternatives></ref><ref id="cit72"><label>72</label><citation-alternatives><mixed-citation xml:lang="ru">Garsen M, Rops AL, Dijkman H et al. Cathepsin L is crucial for the development of early experimental diabetic nephropathy. Kidney Int 2016; 90 (5): 1012-1022. Doi: 10.1016/j.kint.2016.06.035</mixed-citation><mixed-citation xml:lang="en">Garsen M, Rops AL, Dijkman H et al. Cathepsin L is crucial for the development of early experimental diabetic nephropathy. Kidney Int 2016; 90 (5): 1012-1022. Doi: 10.1016/j.kint.2016.06.035</mixed-citation></citation-alternatives></ref><ref id="cit73"><label>73</label><citation-alternatives><mixed-citation xml:lang="ru">Gil N, Goldberg R, Neuman T et al. Heparanase is essential for the development of diabetic nephropathy in mice. Diabetes 2012; 61 (1): 208-216. Doi: 10.2337/db11-1024</mixed-citation><mixed-citation xml:lang="en">Gil N, Goldberg R, Neuman T et al. Heparanase is essential for the development of diabetic nephropathy in mice. Diabetes 2012; 61 (1): 208-216. Doi: 10.2337/db11-1024</mixed-citation></citation-alternatives></ref><ref id="cit74"><label>74</label><citation-alternatives><mixed-citation xml:lang="ru">Wijnhoven TJ, Lensen JF, Rops AL et al. Aberrant heparan sulfate profile in the human diabetic kidney offers new clues for therapeutic glycomimetics. Am J Kidney Dis 2006; 48 (2): 250-261. Doi: 10.1053/j.ajkd.2006.05.003</mixed-citation><mixed-citation xml:lang="en">Wijnhoven TJ, Lensen JF, Rops AL et al. Aberrant heparan sulfate profile in the human diabetic kidney offers new clues for therapeutic glycomimetics. Am J Kidney Dis 2006; 48 (2): 250-261. Doi: 10.1053/j.ajkd.2006.05.003</mixed-citation></citation-alternatives></ref><ref id="cit75"><label>75</label><citation-alternatives><mixed-citation xml:lang="ru">Wijnhoven TJ, van den Hoven MJ, Ding H et al. Heparanase induces a different loss of heparan sulphate domains in overt diabetic nephropathy. Diabetologia 2008; 51 (2): 372-382. Doi: 10.1007/s00125-007-0879-6</mixed-citation><mixed-citation xml:lang="en">Wijnhoven TJ, van den Hoven MJ, Ding H et al. Heparanase induces a different loss of heparan sulphate domains in overt diabetic nephropathy. Diabetologia 2008; 51 (2): 372-382. Doi: 10.1007/s00125-007-0879-6</mixed-citation></citation-alternatives></ref><ref id="cit76"><label>76</label><citation-alternatives><mixed-citation xml:lang="ru">Holt RC, Webb NJ, Ralph S et al. Heparanase activity is dys-regulated in children with steroid-sensitive nephritic syndrome. Kidney Int 2005; 67 (1): 122-129. Doi: 10.1111/j.1523-1755.2005.00062.x</mixed-citation><mixed-citation xml:lang="en">Holt RC, Webb NJ, Ralph S et al. Heparanase activity is dys-regulated in children with steroid-sensitive nephritic syndrome. Kidney Int 2005; 67 (1): 122-129. Doi: 10.1111/j.1523-1755.2005.00062.x</mixed-citation></citation-alternatives></ref><ref id="cit77"><label>77</label><citation-alternatives><mixed-citation xml:lang="ru">Rops AL, van den Hoven MJ, Veldman BA et al. Urinary heparanase activity in patients with type 1 and 2 diabetes. Nephrol Dial Transplant 2012; 27 (7): 2853-2861. Doi: 10.1093/ndt/gfr732</mixed-citation><mixed-citation xml:lang="en">Rops AL, van den Hoven MJ, Veldman BA et al. Urinary heparanase activity in patients with type 1 and 2 diabetes. Nephrol Dial Transplant 2012; 27 (7): 2853-2861. Doi: 10.1093/ndt/gfr732</mixed-citation></citation-alternatives></ref><ref id="cit78"><label>78</label><citation-alternatives><mixed-citation xml:lang="ru">Singh A, Satchell SC, Neal CR et al. Glomerular endothelial glycocalyx constitutes a barrier to protein permeability. J Am Soc Nephrol 2007; 18 (11): 2885-2893. Doi: 10.1681/ASN.2007010119</mixed-citation><mixed-citation xml:lang="en">Singh A, Satchell SC, Neal CR et al. Glomerular endothelial glycocalyx constitutes a barrier to protein permeability. J Am Soc Nephrol 2007; 18 (11): 2885-2893. Doi: 10.1681/ASN.2007010119</mixed-citation></citation-alternatives></ref><ref id="cit79"><label>79</label><citation-alternatives><mixed-citation xml:lang="ru">Jn H, Zhou S. The functions of heparanase in human diseases. Mini Rev Med Chem 2007; 17:541-548. Doi: 10.2174/1389 557516666161101143643</mixed-citation><mixed-citation xml:lang="en">Jn H, Zhou S. The functions of heparanase in human diseases. Mini Rev Med Chem 2007; 17:541-548. Doi: 10.2174/1389 557516666161101143643</mixed-citation></citation-alternatives></ref><ref id="cit80"><label>80</label><citation-alternatives><mixed-citation xml:lang="ru">Levidiotis V, Freeman C, Punler M et al. A synthetic hepara-nase inhibitor reduces proteinuria in passive Heymann nephritis. J Am Soc Nephrol 2004; 15 (11): 2882-2892. Doi: 10.1097/01.ASN.0000142426.55612.6D</mixed-citation><mixed-citation xml:lang="en">Levidiotis V, Freeman C, Punler M et al. A synthetic hepara-nase inhibitor reduces proteinuria in passive Heymann nephritis. J Am Soc Nephrol 2004; 15 (11): 2882-2892. Doi: 10.1097/01.ASN.0000142426.55612.6D</mixed-citation></citation-alternatives></ref><ref id="cit81"><label>81</label><citation-alternatives><mixed-citation xml:lang="ru">Raats CJI, van den Born J, Berden JHM. Glomerular heparin sulfate alterations: Mechanisms and relevance for proteinuria. Kidney Int 2000; 57 (2): 385-400. Doi: 10.1046/j.1523-1755.2000.00858.x</mixed-citation><mixed-citation xml:lang="en">Raats CJI, van den Born J, Berden JHM. Glomerular heparin sulfate alterations: Mechanisms and relevance for proteinuria. Kidney Int 2000; 57 (2): 385-400. Doi: 10.1046/j.1523-1755.2000.00858.x</mixed-citation></citation-alternatives></ref><ref id="cit82"><label>82</label><citation-alternatives><mixed-citation xml:lang="ru">Singh A, Ramnath RD, Foster RR et al. Reactive oxygen species modulate the barrier function of the human glomerular endothelial glycocalyx. PLoS One 2013; 8 (2): e55852. Doi: 10.1371/journal.pone.0055852</mixed-citation><mixed-citation xml:lang="en">Singh A, Ramnath RD, Foster RR et al. Reactive oxygen species modulate the barrier function of the human glomerular endothelial glycocalyx. PLoS One 2013; 8 (2): e55852. Doi: 10.1371/journal.pone.0055852</mixed-citation></citation-alternatives></ref><ref id="cit83"><label>83</label><citation-alternatives><mixed-citation xml:lang="ru">Forbes JM, Coughlan MT, Cooper ME. Oxidative stress as a major culprit in kidney disease in diabetes. Diabetes 2008; 57 (6): 1446-1454. Doi: 10.2337/db08-0057</mixed-citation><mixed-citation xml:lang="en">Forbes JM, Coughlan MT, Cooper ME. Oxidative stress as a major culprit in kidney disease in diabetes. Diabetes 2008; 57 (6): 1446-1454. Doi: 10.2337/db08-0057</mixed-citation></citation-alternatives></ref><ref id="cit84"><label>84</label><citation-alternatives><mixed-citation xml:lang="ru">Raats CJI, Bakker MAH, van den Born J, Berden JHM. Hydroxyl radicals depolymerize glomerular heparin sulfate in vitro and in experimental nephritic syndrome. J Biol Chem 1997; 272 (42): 26734-26741</mixed-citation><mixed-citation xml:lang="en">Raats CJI, Bakker MAH, van den Born J, Berden JHM. Hydroxyl radicals depolymerize glomerular heparin sulfate in vitro and in experimental nephritic syndrome. J Biol Chem 1997; 272 (42): 26734-26741</mixed-citation></citation-alternatives></ref><ref id="cit85"><label>85</label><citation-alternatives><mixed-citation xml:lang="ru">Rops AL, van der Vlag, Jensen JF et al. Heparan sulfate proteoglycans in glomerular inflammation. Kidney Int 2004; 65 (3): 768-785. Doi: 10.1111/j.1523-1755.2004.00451.x</mixed-citation><mixed-citation xml:lang="en">Rops AL, van der Vlag, Jensen JF et al. Heparan sulfate proteoglycans in glomerular inflammation. Kidney Int 2004; 65 (3): 768-785. Doi: 10.1111/j.1523-1755.2004.00451.x</mixed-citation></citation-alternatives></ref><ref id="cit86"><label>86</label><citation-alternatives><mixed-citation xml:lang="ru">Klebanoff SJ, Kinsella MG, Wight TN. Degradation of endothelial cell matrix heparan sulfate proteoglycan by elastase and the myeloperoxidase-H2O2-chloride system. Am J Pathol 1993; 143 (3): 907-917</mixed-citation><mixed-citation xml:lang="en">Klebanoff SJ, Kinsella MG, Wight TN. Degradation of endothelial cell matrix heparan sulfate proteoglycan by elastase and the myeloperoxidase-H2O2-chloride system. Am J Pathol 1993; 143 (3): 907-917</mixed-citation></citation-alternatives></ref><ref id="cit87"><label>87</label><citation-alternatives><mixed-citation xml:lang="ru">Panasyuk K, Frati E, Ribault D, Mitrovic D. Effect of reactive oxygen species on the biosynthesis and structure of newly synthesized proteoglycans.Free Radic Biol Med 1994; 16 (2): 157-167</mixed-citation><mixed-citation xml:lang="en">Panasyuk K, Frati E, Ribault D, Mitrovic D. Effect of reactive oxygen species on the biosynthesis and structure of newly synthesized proteoglycans.Free Radic Biol Med 1994; 16 (2): 157-167</mixed-citation></citation-alternatives></ref><ref id="cit88"><label>88</label><citation-alternatives><mixed-citation xml:lang="ru">Moseley R, Waddington R, EvansP et al. The chemical modification of glycosaminoglycan structure by oxygen-derived species in vitro. Biochim Biophys Acta 1995; 1244 (2-3): 245-252</mixed-citation><mixed-citation xml:lang="en">Moseley R, Waddington R, EvansP et al. The chemical modification of glycosaminoglycan structure by oxygen-derived species in vitro. Biochim Biophys Acta 1995; 1244 (2-3): 245-252</mixed-citation></citation-alternatives></ref><ref id="cit89"><label>89</label><citation-alternatives><mixed-citation xml:lang="ru">Edge AS, Spiro RG. A specific structural alteration in the heparin sulphate of human glomerular basement membrane in diabetes. Diabetologia 2000; 43 (8): 1056-1059. Doi: 10.1007/s001250051489</mixed-citation><mixed-citation xml:lang="en">Edge AS, Spiro RG. A specific structural alteration in the heparin sulphate of human glomerular basement membrane in diabetes. Diabetologia 2000; 43 (8): 1056-1059. Doi: 10.1007/s001250051489</mixed-citation></citation-alternatives></ref><ref id="cit90"><label>90</label><citation-alternatives><mixed-citation xml:lang="ru">Lowik MM, Hol FA, Steenbergen EJ et al. Mitochondrial tRNALeu (UUR) mutation in a patient with steroid-resistant nephrotic syndrome and focal segmental glomerulosclerosis. Nephrol Dial Transplant 2005; 20 (2): 336-341. Doi: 10.1093/ndt/gfh546</mixed-citation><mixed-citation xml:lang="en">Lowik MM, Hol FA, Steenbergen EJ et al. Mitochondrial tRNALeu (UUR) mutation in a patient with steroid-resistant nephrotic syndrome and focal segmental glomerulosclerosis. Nephrol Dial Transplant 2005; 20 (2): 336-341. Doi: 10.1093/ndt/gfh546</mixed-citation></citation-alternatives></ref><ref id="cit91"><label>91</label><citation-alternatives><mixed-citation xml:lang="ru">Wang W, Wang X Long J et al. Mitochondrial fission triggered by hyperglycemia is mediated by ROCK1 activation in podocytes and endothelial cells. Cell Metab 2012; 15 (2): 186-200. Doi: 10.1016/j.cmet.2012.01.009</mixed-citation><mixed-citation xml:lang="en">Wang W, Wang X Long J et al. Mitochondrial fission triggered by hyperglycemia is mediated by ROCK1 activation in podocytes and endothelial cells. Cell Metab 2012; 15 (2): 186-200. Doi: 10.1016/j.cmet.2012.01.009</mixed-citation></citation-alternatives></ref><ref id="cit92"><label>92</label><citation-alternatives><mixed-citation xml:lang="ru">Li M, Rosenfeld L, Vilar RE, Cowman MK. Degradation of hyaluronan by peroxynitrite. Arch Biochem Biophys 1997; 341 (2): 245-250. Doi: 10.1006/abbi.1997.9970</mixed-citation><mixed-citation xml:lang="en">Li M, Rosenfeld L, Vilar RE, Cowman MK. Degradation of hyaluronan by peroxynitrite. Arch Biochem Biophys 1997; 341 (2): 245-250. Doi: 10.1006/abbi.1997.9970</mixed-citation></citation-alternatives></ref><ref id="cit93"><label>93</label><citation-alternatives><mixed-citation xml:lang="ru">Vassilou P, Tay M, Comper WD. Partial ischemia and proteinuria during isolated kidney perfusion is accompanied by the release of vascular [35S] heparin sulfate. Biochem Int 1989; 19 (6): 1241-1251</mixed-citation><mixed-citation xml:lang="en">Vassilou P, Tay M, Comper WD. Partial ischemia and proteinuria during isolated kidney perfusion is accompanied by the release of vascular [35S] heparin sulfate. Biochem Int 1989; 19 (6): 1241-1251</mixed-citation></citation-alternatives></ref><ref id="cit94"><label>94</label><citation-alternatives><mixed-citation xml:lang="ru">Tan S, YokoyamaX Dickens E et al. Xanthine oxidase activity in the circulation of rats following hemorrhagic shock. Free Radic Biol Med 1993; 15 (4): 407-414</mixed-citation><mixed-citation xml:lang="en">Tan S, YokoyamaX Dickens E et al. Xanthine oxidase activity in the circulation of rats following hemorrhagic shock. Free Radic Biol Med 1993; 15 (4): 407-414</mixed-citation></citation-alternatives></ref><ref id="cit95"><label>95</label><citation-alternatives><mixed-citation xml:lang="ru">Гавриленко ТИ, Рыжкова НА, Пархоменко АН. Сосудистый эндотелиальный фактор роста в клинике внутренних заболеваний и его патогенетическое значение. УкраНський кард1олопчний журнал 2011; (4): 87-95</mixed-citation><mixed-citation xml:lang="en">GavriilenkoTI, Rizhkova NA, Parkhomenko AN. Sosudistyj endotelisl’niy factor rosta v klinike vnutrennikh zabolevanij i ego patogeneticheskoe znachenie. Ukrainskij kardiologichnij zhurnal 2011; (4): 87-95 (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit96"><label>96</label><citation-alternatives><mixed-citation xml:lang="ru">Жариков АЮ, Щекочихина РО. Диабетическая нефропатия. Современный взгляд на проблему. Бюлл мед науки 2018; (2): 24-31</mixed-citation><mixed-citation xml:lang="en">Zharikov AYu, Schekochikhina RO.Diabeticheskaja nefropatija. Sovremennyj vzglyad na problemu. Byullmed nauki 2018; (2): 24-31 (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit97"><label>97</label><citation-alternatives><mixed-citation xml:lang="ru">Eremina V, Baelde HJ, Quaggin SE. Role of the VEGF-A signaling pathway in the glomerulus: evidence for crosstalk between components of the glomerular filtration barrier. Nephron Physiol2007; 106: 32-37. Doi: 10.1159/000101798</mixed-citation><mixed-citation xml:lang="en">Eremina V, Baelde HJ, Quaggin SE. Role of the VEGF-A signaling pathway in the glomerulus: evidence for crosstalk between components of the glomerular filtration barrier. Nephron Physiol2007; 106: 32-37. Doi: 10.1159/000101798</mixed-citation></citation-alternatives></ref><ref id="cit98"><label>98</label><citation-alternatives><mixed-citation xml:lang="ru">Eremina V, Sood M, Haigh J et al. Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases. J Clin Invest 2003; 111 (5): 707-716. Doi: 10.1172/JCI17423</mixed-citation><mixed-citation xml:lang="en">Eremina V, Sood M, Haigh J et al. Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases. J Clin Invest 2003; 111 (5): 707-716. Doi: 10.1172/JCI17423</mixed-citation></citation-alternatives></ref><ref id="cit99"><label>99</label><citation-alternatives><mixed-citation xml:lang="ru">Sugimoto H, Hamano X Charytan D et al. Neutralization of circulating vascular endothelial growth factor (VEGF) by anti-VEGF antibodies and soluble VEGF receptor 1 (sFlt-1) induces proteinuria. J Biol Chem 2003; 278 (15): 12605-12608. Doi: 10.1074/jbc.C300012200</mixed-citation><mixed-citation xml:lang="en">Sugimoto H, Hamano X Charytan D et al. Neutralization of circulating vascular endothelial growth factor (VEGF) by anti-VEGF antibodies and soluble VEGF receptor 1 (sFlt-1) induces proteinuria. J Biol Chem 2003; 278 (15): 12605-12608. Doi: 10.1074/jbc.C300012200</mixed-citation></citation-alternatives></ref><ref id="cit100"><label>100</label><citation-alternatives><mixed-citation xml:lang="ru">Veron D, Reidy K, MarlierA et al. Induction of podocyte VEGF164 overexpression at different stages of development causes congenital nephrosis or steroid-resistant nephrotic syndrome. Am J Pathol 2010; 177 (5): 2225-2233. Doi: 10.2353/ajpath.2010.091146</mixed-citation><mixed-citation xml:lang="en">Veron D, Reidy K, MarlierA et al. Induction of podocyte VEGF164 overexpression at different stages of development causes congenital nephrosis or steroid-resistant nephrotic syndrome. Am J Pathol 2010; 177 (5): 2225-2233. Doi: 10.2353/ajpath.2010.091146</mixed-citation></citation-alternatives></ref><ref id="cit101"><label>101</label><citation-alternatives><mixed-citation xml:lang="ru">Veron D, Reidy KJ, Bertuccio C et al. Overexpression of VEGF-A in podocytes of adult mice causes glomerular disease. Kidney Int 2010; 77 (11): 989-999. Doi: 10.1038/ki.2010.64</mixed-citation><mixed-citation xml:lang="en">Veron D, Reidy KJ, Bertuccio C et al. Overexpression of VEGF-A in podocytes of adult mice causes glomerular disease. Kidney Int 2010; 77 (11): 989-999. Doi: 10.1038/ki.2010.64</mixed-citation></citation-alternatives></ref><ref id="cit102"><label>102</label><citation-alternatives><mixed-citation xml:lang="ru">Chiarelli F, Spagnoli A, Basciani F et al. Vascular endothelial growth factor (VEGF) in children, adolescents and young adults with Type 1 diabetes mellitus: relation to glycaemic control and microvascular complications. Diabet Med 2000; 17 (9): 650-656</mixed-citation><mixed-citation xml:lang="en">Chiarelli F, Spagnoli A, Basciani F et al. Vascular endothelial growth factor (VEGF) in children, adolescents and young adults with Type 1 diabetes mellitus: relation to glycaemic control and microvascular complications. Diabet Med 2000; 17 (9): 650-656</mixed-citation></citation-alternatives></ref><ref id="cit103"><label>103</label><citation-alternatives><mixed-citation xml:lang="ru">Hoving P, Tarnow L, Oestergaard PB, Parving HH. Elevated vascular endothelial growth factor in type 1 diabetic patients with diabetic nephropathy. Kidney Int 2000; 75: S56-S61</mixed-citation><mixed-citation xml:lang="en">Hoving P, Tarnow L, Oestergaard PB, Parving HH. Elevated vascular endothelial growth factor in type 1 diabetic patients with diabetic nephropathy. Kidney Int 2000; 75: S56-S61</mixed-citation></citation-alternatives></ref><ref id="cit104"><label>104</label><citation-alternatives><mixed-citation xml:lang="ru">Fu J, Lee K, Chuang PY et al. Glomerular endothelial cell injury and cross talk in diabetic kidney disease. Am J Physiol Renal Physiol 2014; 308 (4): F287-F297. Doi: 10.1152/ajprenal. 00533.2014</mixed-citation><mixed-citation xml:lang="en">Fu J, Lee K, Chuang PY et al. Glomerular endothelial cell injury and cross talk in diabetic kidney disease. Am J Physiol Renal Physiol 2014; 308 (4): F287-F297. Doi: 10.1152/ajprenal. 00533.2014</mixed-citation></citation-alternatives></ref><ref id="cit105"><label>105</label><citation-alternatives><mixed-citation xml:lang="ru">Ostalska-Nowicka D, Malinska A, Zabel M et al. Nephrotic syndrome unfavorable course correlates with downregulation of podocyte vascular endothelial growth factor receptor (VEGF)-2. Folia Histochem Cytobiol 2011; 49 (5): 472-478. Doi: 10.5603/FHC.2011.0067</mixed-citation><mixed-citation xml:lang="en">Ostalska-Nowicka D, Malinska A, Zabel M et al. Nephrotic syndrome unfavorable course correlates with downregulation of podocyte vascular endothelial growth factor receptor (VEGF)-2. Folia Histochem Cytobiol 2011; 49 (5): 472-478. Doi: 10.5603/FHC.2011.0067</mixed-citation></citation-alternatives></ref><ref id="cit106"><label>106</label><citation-alternatives><mixed-citation xml:lang="ru">de VrieseAS, Tilton RG, ElgerM et al. Antibodies against vascular endothelial growth factor improve early renal dysfunction in experimental diabetes. J Am Soc Nephrol 2001; 12 (5): 993-1000</mixed-citation><mixed-citation xml:lang="en">de VrieseAS, Tilton RG, ElgerM et al. Antibodies against vascular endothelial growth factor improve early renal dysfunction in experimental diabetes. J Am Soc Nephrol 2001; 12 (5): 993-1000</mixed-citation></citation-alternatives></ref><ref id="cit107"><label>107</label><citation-alternatives><mixed-citation xml:lang="ru">Cha DR, Kang YS, Han SYet al. Vascular endothelual growth factor is increased during early stage of diabetic nephropathy in type II diabetic rats. J Endocrinol 2004; 183 (1): 183-194. Doi: 10.1677/joe.1.05647</mixed-citation><mixed-citation xml:lang="en">Cha DR, Kang YS, Han SYet al. Vascular endothelual growth factor is increased during early stage of diabetic nephropathy in type II diabetic rats. J Endocrinol 2004; 183 (1): 183-194. Doi: 10.1677/joe.1.05647</mixed-citation></citation-alternatives></ref><ref id="cit108"><label>108</label><citation-alternatives><mixed-citation xml:lang="ru">Sung SH, Ziyadeh FN, Wang A et al. Blockade of vascular endothelial growth factor signaling ameliorates diabetic albuminuria in mice. J Am Soc Nephrol 2006; 17 (11): 3093-3104. Doi: 10.1681/ASN.2006010064</mixed-citation><mixed-citation xml:lang="en">Sung SH, Ziyadeh FN, Wang A et al. Blockade of vascular endothelial growth factor signaling ameliorates diabetic albuminuria in mice. J Am Soc Nephrol 2006; 17 (11): 3093-3104. Doi: 10.1681/ASN.2006010064</mixed-citation></citation-alternatives></ref><ref id="cit109"><label>109</label><citation-alternatives><mixed-citation xml:lang="ru">Lindenmeyer MT, Kretzler M, Boicherot A et al. Interstitial vascular rarefaction and reduced VEGF-A expression in human diabetic nephropathy. JAm Soc Nephrol2007; 18 (6): 1765-1776. Doi: 10.1681/ASN.2006121304</mixed-citation><mixed-citation xml:lang="en">Lindenmeyer MT, Kretzler M, Boicherot A et al. Interstitial vascular rarefaction and reduced VEGF-A expression in human diabetic nephropathy. JAm Soc Nephrol2007; 18 (6): 1765-1776. Doi: 10.1681/ASN.2006121304</mixed-citation></citation-alternatives></ref><ref id="cit110"><label>110</label><citation-alternatives><mixed-citation xml:lang="ru">Daniels BS, Hauser EB, Deen WM, Hostetter TH. Glomerular basement membrane: in vitro studies of water and protein perme-ability.Am J Physiol Renal Fluid Electrolyte Physiol 1992; 262 (6 Pt2): F919-F926. Doi: 10.1152/ajprenal.1992.262.6.F919</mixed-citation><mixed-citation xml:lang="en">Daniels BS, Hauser EB, Deen WM, Hostetter TH. Glomerular basement membrane: in vitro studies of water and protein perme-ability.Am J Physiol Renal Fluid Electrolyte Physiol 1992; 262 (6 Pt2): F919-F926. Doi: 10.1152/ajprenal.1992.262.6.F919</mixed-citation></citation-alternatives></ref><ref id="cit111"><label>111</label><citation-alternatives><mixed-citation xml:lang="ru">Bolton GR, Deen WM, Daniels BS. Assesment of the charge selectivity of glomerular basement membrane using Ficoll sulfate. Am J Physiol Renal Physiol 1998; 274 (5): F889-F896. Doi: 10.1152/ajprenal.1998.274.5.F889</mixed-citation><mixed-citation xml:lang="en">Bolton GR, Deen WM, Daniels BS. Assesment of the charge selectivity of glomerular basement membrane using Ficoll sulfate. Am J Physiol Renal Physiol 1998; 274 (5): F889-F896. Doi: 10.1152/ajprenal.1998.274.5.F889</mixed-citation></citation-alternatives></ref><ref id="cit112"><label>112</label><citation-alternatives><mixed-citation xml:lang="ru">Saritas T, Kuppe C, Moeller M. Progress and controversies in unraveling the glomerular filtration mechanism. Curr Opin Nephrol Hypertens 2015; 24 (3): 208-216. Doi: 10.1097/MNH.0000000000000116</mixed-citation><mixed-citation xml:lang="en">Saritas T, Kuppe C, Moeller M. Progress and controversies in unraveling the glomerular filtration mechanism. Curr Opin Nephrol Hypertens 2015; 24 (3): 208-216. Doi: 10.1097/MNH.0000000000000116</mixed-citation></citation-alternatives></ref><ref id="cit113"><label>113</label><citation-alternatives><mixed-citation xml:lang="ru">Pierson M, Cordier J, Hervouuet F, Rauber G. An unusual congenital and familial congenital malformative combination involving the eye and kidney. J Genet Hum 1963; 12: 184-213</mixed-citation><mixed-citation xml:lang="en">Pierson M, Cordier J, Hervouuet F, Rauber G. An unusual congenital and familial congenital malformative combination involving the eye and kidney. J Genet Hum 1963; 12: 184-213</mixed-citation></citation-alternatives></ref><ref id="cit114"><label>114</label><citation-alternatives><mixed-citation xml:lang="ru">Zenker M, Aigner T, Wender O et al. Human laminin beta 2 deficiency causes congenital nephrosis with mesangial sclerosis and distinct eye abnormalities. Hum Mol Genet 2004; 13 (21): 2625-2632. Doi: 10.1093/hmg/ddh284</mixed-citation><mixed-citation xml:lang="en">Zenker M, Aigner T, Wender O et al. Human laminin beta 2 deficiency causes congenital nephrosis with mesangial sclerosis and distinct eye abnormalities. Hum Mol Genet 2004; 13 (21): 2625-2632. Doi: 10.1093/hmg/ddh284</mixed-citation></citation-alternatives></ref><ref id="cit115"><label>115</label><citation-alternatives><mixed-citation xml:lang="ru">Hasselbacher K, Wiggins RC, Matejas V et al. Recessive missense mutations in LAMB2 expand the clinical spectrum of LAMB2-associated disorder. Kidney Int 2006; 70 (6): 1008-1012. Doi: 10.1038/sj.ki.5001679</mixed-citation><mixed-citation xml:lang="en">Hasselbacher K, Wiggins RC, Matejas V et al. Recessive missense mutations in LAMB2 expand the clinical spectrum of LAMB2-associated disorder. Kidney Int 2006; 70 (6): 1008-1012. Doi: 10.1038/sj.ki.5001679</mixed-citation></citation-alternatives></ref><ref id="cit116"><label>116</label><citation-alternatives><mixed-citation xml:lang="ru">Suh JH, Miner JH. The glomerular basement membranes as a barrier to albumin. Nat Rev Nephrol 2014; 9 (8): 470-477</mixed-citation><mixed-citation xml:lang="en">Suh JH, Miner JH. The glomerular basement membranes as a barrier to albumin. Nat Rev Nephrol 2014; 9 (8): 470-477</mixed-citation></citation-alternatives></ref><ref id="cit117"><label>117</label><citation-alternatives><mixed-citation xml:lang="ru">Jarad G, Cunningham J, Shaw AS, Miner JH. Proteinuria precedes podocyte abnormalities in Lamb2-/- mice, implicating the glomerular basement membrane as an albumin barrier. J Clin Invest 2006; 116 (8): 2272-2279. Doi: 10.1172/JCI28414</mixed-citation><mixed-citation xml:lang="en">Jarad G, Cunningham J, Shaw AS, Miner JH. Proteinuria precedes podocyte abnormalities in Lamb2-/- mice, implicating the glomerular basement membrane as an albumin barrier. J Clin Invest 2006; 116 (8): 2272-2279. Doi: 10.1172/JCI28414</mixed-citation></citation-alternatives></ref><ref id="cit118"><label>118</label><citation-alternatives><mixed-citation xml:lang="ru">Chen YM, Liapis H. Focal segmental glomerulosclerosis: molecular genetics and targeted therapies. BMC Nephrology 2015; 16 (101): 1-10. Doi:10.1186/s12882-015-0090-9</mixed-citation><mixed-citation xml:lang="en">Chen YM, Liapis H. Focal segmental glomerulosclerosis: molecular genetics and targeted therapies. BMC Nephrology 2015; 16 (101): 1-10. Doi:10.1186/s12882-015-0090-9</mixed-citation></citation-alternatives></ref><ref id="cit119"><label>119</label><citation-alternatives><mixed-citation xml:lang="ru">Abrahamson DR, Isom K, Roach E et al. Laminin compensation in collagen alpha 3(IV) knockout (Alport) glomeruli contributes to permeability defects. J Am Soc Nephrol 2007; 18 (9): 2465-2472. Doi: 10.1681/ASN.2007030328</mixed-citation><mixed-citation xml:lang="en">Abrahamson DR, Isom K, Roach E et al. Laminin compensation in collagen alpha 3(IV) knockout (Alport) glomeruli contributes to permeability defects. J Am Soc Nephrol 2007; 18 (9): 2465-2472. Doi: 10.1681/ASN.2007030328</mixed-citation></citation-alternatives></ref><ref id="cit120"><label>120</label><citation-alternatives><mixed-citation xml:lang="ru">Kanwar YS, Linker A, Farquhar MG. Increased permeability of the glomerular basement membrane to ferritin after removal of glycosaminoglycans (heparan sulfate) by enzyme digestion. J Cell Biol 1980; 86 (2): 688-693</mixed-citation><mixed-citation xml:lang="en">Kanwar YS, Linker A, Farquhar MG. Increased permeability of the glomerular basement membrane to ferritin after removal of glycosaminoglycans (heparan sulfate) by enzyme digestion. J Cell Biol 1980; 86 (2): 688-693</mixed-citation></citation-alternatives></ref><ref id="cit121"><label>121</label><citation-alternatives><mixed-citation xml:lang="ru">Van den Born J, van den Heuvel LP, Bakker MA et al. A monoclonal antibody against GBM heparan sulfate induces an acute selective proteinuria in rats. Kidney Int 1992; 41 (1): 115-123</mixed-citation><mixed-citation xml:lang="en">Van den Born J, van den Heuvel LP, Bakker MA et al. A monoclonal antibody against GBM heparan sulfate induces an acute selective proteinuria in rats. Kidney Int 1992; 41 (1): 115-123</mixed-citation></citation-alternatives></ref><ref id="cit122"><label>122</label><citation-alternatives><mixed-citation xml:lang="ru">Raats CJ, Luca ME, Bakker MA et al. Reduction in glomerular heparan sulfate correlates with complement deposition and albuminuria in active Heymann nephritis. J Am Soc Nephrol 1999; 10 (8): 1689-1699</mixed-citation><mixed-citation xml:lang="en">Raats CJ, Luca ME, Bakker MA et al. Reduction in glomerular heparan sulfate correlates with complement deposition and albuminuria in active Heymann nephritis. J Am Soc Nephrol 1999; 10 (8): 1689-1699</mixed-citation></citation-alternatives></ref><ref id="cit123"><label>123</label><citation-alternatives><mixed-citation xml:lang="ru">Lauer ME, Hascall VC, Wang A. Heparan sulfate analysis from diabetic rat glomeruli. J Bio lChem 2007; 282 (2): 843-852. Doi: 10.1074/jbc.M6088232200</mixed-citation><mixed-citation xml:lang="en">Lauer ME, Hascall VC, Wang A. Heparan sulfate analysis from diabetic rat glomeruli. J Bio lChem 2007; 282 (2): 843-852. Doi: 10.1074/jbc.M6088232200</mixed-citation></citation-alternatives></ref><ref id="cit124"><label>124</label><citation-alternatives><mixed-citation xml:lang="ru">An X, Zhang L, YuanY et al. Hyperoside pre-treatment prevents glomerular basement membrane damage in diabetic nephropathy by inhibiting podocyte heparanase expression. Sci Rep 2017;7 (1):6413. Doi: 10.1038/s41598-017-06844-2</mixed-citation><mixed-citation xml:lang="en">An X, Zhang L, YuanY et al. Hyperoside pre-treatment prevents glomerular basement membrane damage in diabetic nephropathy by inhibiting podocyte heparanase expression. Sci Rep 2017;7 (1):6413. Doi: 10.1038/s41598-017-06844-2</mixed-citation></citation-alternatives></ref><ref id="cit125"><label>125</label><citation-alternatives><mixed-citation xml:lang="ru">Luo W, Olaru F, Miner JH et al. Alternative pathway is essential for glomerular complement activation and proteinuria in a mouse model of membranous nephropathy. Front Immun 2018; 9: 1433. Doi: 10.3389/fimmu.2018.01433</mixed-citation><mixed-citation xml:lang="en">Luo W, Olaru F, Miner JH et al. Alternative pathway is essential for glomerular complement activation and proteinuria in a mouse model of membranous nephropathy. Front Immun 2018; 9: 1433. Doi: 10.3389/fimmu.2018.01433</mixed-citation></citation-alternatives></ref><ref id="cit126"><label>126</label><citation-alternatives><mixed-citation xml:lang="ru">Kim HJ, Hong YH, Kim YJ et al. Anti-heparan sulfate proteoglycans in lupus nephritis. Lupus 2016; 0: 1-10</mixed-citation><mixed-citation xml:lang="en">Kim HJ, Hong YH, Kim YJ et al. Anti-heparan sulfate proteoglycans in lupus nephritis. Lupus 2016; 0: 1-10</mixed-citation></citation-alternatives></ref><ref id="cit127"><label>127</label><citation-alternatives><mixed-citation xml:lang="ru">van den BornJ, Pisa B, Bakker MA etal. No change in glomerular heparan sulfatestructure in early human and experimental diabetic nephropathy. J Biol Chem 2006; 281 (40): 29606-29613. Doi: 10.1074/jbc.M601552200</mixed-citation><mixed-citation xml:lang="en">van den BornJ, Pisa B, Bakker MA etal. No change in glomerular heparan sulfatestructure in early human and experimental diabetic nephropathy. J Biol Chem 2006; 281 (40): 29606-29613. Doi: 10.1074/jbc.M601552200</mixed-citation></citation-alternatives></ref><ref id="cit128"><label>128</label><citation-alternatives><mixed-citation xml:lang="ru">Wijnhoven TJ, Lensen JF, Wismans RG et al. In vivo degradation of heparin sulfates in the glomerular basement membrane does not result in proteinuria. J Am Soc Nephrol 2007; 18 (3): 823-832. Doi: 10.1681/ASN.2006070692</mixed-citation><mixed-citation xml:lang="en">Wijnhoven TJ, Lensen JF, Wismans RG et al. In vivo degradation of heparin sulfates in the glomerular basement membrane does not result in proteinuria. J Am Soc Nephrol 2007; 18 (3): 823-832. Doi: 10.1681/ASN.2006070692</mixed-citation></citation-alternatives></ref><ref id="cit129"><label>129</label><citation-alternatives><mixed-citation xml:lang="ru">Harvey SJ, Jarad G, Cunningham J et al. Disruption on glomerular basement membrane charge through podocyte-specific mutation of agrin does not alter glomerular permselectivity. Am J Pathol 2007; 171 (1): 139-152. Doi: 10.2353/ajpath.2007.061116</mixed-citation><mixed-citation xml:lang="en">Harvey SJ, Jarad G, Cunningham J et al. Disruption on glomerular basement membrane charge through podocyte-specific mutation of agrin does not alter glomerular permselectivity. Am J Pathol 2007; 171 (1): 139-152. Doi: 10.2353/ajpath.2007.061116</mixed-citation></citation-alternatives></ref><ref id="cit130"><label>130</label><citation-alternatives><mixed-citation xml:lang="ru">Бобкова ИН, Кахсуруева ПА, Ставровская ЕВ, Филатова ЕЕ. Эволюция в понимании патогенеза идиопатической мембранозной нефропатии: от экспериментальных моделей к клинике. Альманах клин мед 2017; 45 (7): 553-564. Doi: 10.18786/2072-0505-2017-45-7-553-564</mixed-citation><mixed-citation xml:lang="en">Bobkova IN, Kakhsurueva PA, Stavrovskaja EV, Filatova E E. Evolyutsija v ponimanii patogeneza idiopaticheskoj membranoznoj nefropatii: ot eksperimental’nykh modelej k klinike. Al'manakh kiln med 2017; 45 (7): 553-564. Doi: 10.18786/2072-0505-2017-45-7-553-564 (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit131"><label>131</label><citation-alternatives><mixed-citation xml:lang="ru">Kestila M, Morita T, Mannikko M et al. Positionally cloned gene for a novel glomerular protein-nephrin-is mutated in congenital nephrotic syndrome. Mol Cell 1998; 1 (4): 575-582</mixed-citation><mixed-citation xml:lang="en">Kestila M, Morita T, Mannikko M et al. Positionally cloned gene for a novel glomerular protein-nephrin-is mutated in congenital nephrotic syndrome. Mol Cell 1998; 1 (4): 575-582</mixed-citation></citation-alternatives></ref><ref id="cit132"><label>132</label><citation-alternatives><mixed-citation xml:lang="ru">Binczak-Kuleta A, Rubik J, Litwin M etal. Retrospective mutational analysis of NPHS1, NPHS2, WT1 and LAMB2 in children with steroid-resistant focal segmental glomerulosclerosis - a singlecentre experience. Bosn J Basic Med Sci 2014; 14 (2): 89-93. Doi: 10.17305/bjbms.2014.2270</mixed-citation><mixed-citation xml:lang="en">Binczak-Kuleta A, Rubik J, Litwin M etal. Retrospective mutational analysis of NPHS1, NPHS2, WT1 and LAMB2 in children with steroid-resistant focal segmental glomerulosclerosis - a singlecentre experience. Bosn J Basic Med Sci 2014; 14 (2): 89-93. Doi: 10.17305/bjbms.2014.2270</mixed-citation></citation-alternatives></ref><ref id="cit133"><label>133</label><citation-alternatives><mixed-citation xml:lang="ru">Морозов СЛ, Длин ВВ, Садыков АР и др. Механизмы резистентности к иммуносупрессивной терапии у пациентов с нефротическим синдромом. Рос вестн перинатол и педиатр 2017; 62 (4): 19-24. doc. 10.21508/1027-4065-2017-62-4-19-24</mixed-citation><mixed-citation xml:lang="en">Morozov SL, Dlin VV, Sadykov AR i dr. Mekhanizmy rezistentnosty k immunosupressivnoj terapii u patsientov s nefroticheskim syndromom. Ros vestn perinatolipediatr 2017; 62 (4): 19-24. doc. 10.21508/1027-4065-2017-62-4-19-24 (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit134"><label>134</label><citation-alternatives><mixed-citation xml:lang="ru">Ranganathan S. Pathology of podocytopathies causing nephrotic syndrome in children. Front Pediatr 2016; 4: 32. Doi: 10.3389/fped.2016.00032</mixed-citation><mixed-citation xml:lang="en">Ranganathan S. Pathology of podocytopathies causing nephrotic syndrome in children. Front Pediatr 2016; 4: 32. Doi: 10.3389/fped.2016.00032</mixed-citation></citation-alternatives></ref><ref id="cit135"><label>135</label><citation-alternatives><mixed-citation xml:lang="ru">Kawachi H, Koike H, Kurihara H et al. Cloning of rat nephron: expression in developing glomeruli and in proteinuric states. Kidney Int 2000; 57 (5): 1949-1961. Doi: 10.1046/j.1523-1755.2000.00044.x</mixed-citation><mixed-citation xml:lang="en">Kawachi H, Koike H, Kurihara H et al. Cloning of rat nephron: expression in developing glomeruli and in proteinuric states. Kidney Int 2000; 57 (5): 1949-1961. Doi: 10.1046/j.1523-1755.2000.00044.x</mixed-citation></citation-alternatives></ref><ref id="cit136"><label>136</label><citation-alternatives><mixed-citation xml:lang="ru">Luimula P, Ahola H, Wang SX et al.Nephrin in experimental glomerular disease. Kidney Int 2000; 58 (4): 1461-1468. Doi: 10.1046/j.1523-1755.2000.00308.x</mixed-citation><mixed-citation xml:lang="en">Luimula P, Ahola H, Wang SX et al.Nephrin in experimental glomerular disease. Kidney Int 2000; 58 (4): 1461-1468. Doi: 10.1046/j.1523-1755.2000.00308.x</mixed-citation></citation-alternatives></ref><ref id="cit137"><label>137</label><citation-alternatives><mixed-citation xml:lang="ru">Yjan H, Takeuchi E, Taylor GA et al. Nephrin dissociates from actin, and its expression is reduced in early experimental membranous nephropathy. J Am Soc Nephrol 2002; 13 (4): 946-956.</mixed-citation><mixed-citation xml:lang="en">Yjan H, Takeuchi E, Taylor GA et al. Nephrin dissociates from actin, and its expression is reduced in early experimental membranous nephropathy. J Am Soc Nephrol 2002; 13 (4): 946-956.</mixed-citation></citation-alternatives></ref><ref id="cit138"><label>138</label><citation-alternatives><mixed-citation xml:lang="ru">Наушбаева АЕ, Абеуова БА, Чингаева ГН и др. Генетически обусловленные варианты стероидрезистентного нефротического синдрома. Вестн КАЗНМУ 2012; (2): 214-215</mixed-citation><mixed-citation xml:lang="en">Naushbaeva AE, Abeuova BA, Chingaeva GN i dr. Genetichesky obuslovlennye varianty steroidrezistentnogo nefroticheskogo sin-droma. Vestn KAZNMU 2012; (2): 214-215 (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit139"><label>139</label><citation-alternatives><mixed-citation xml:lang="ru">Игнатова МС, Длин ВВ. Нефротический синдром: прошлое, настоящее и будущее. Рос вестн перинатол и педиатр 2017; 62 (6): 29-44. Doi: 10.21508/1027-4065-2017-62-6-29-44</mixed-citation><mixed-citation xml:lang="en">Ignatova MS, Dlin VV. Nefroticheskij syndrom: proshloe, nas-toyzschee i buduschee. Ros vest nperinatol i pediatr 2017; 62 (6): 29-44. Doi: 10.21508/1027-4065-2017-62-6-29-44 (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit140"><label>140</label><citation-alternatives><mixed-citation xml:lang="ru">Kim JM, Wu H, Green G et al. CD2-associated protein haploinsufficiency is linked to glomerular disease susceptibility. Science 2003; 300 (5623): 1298-1300. Doi: 10.1126/science.1081068</mixed-citation><mixed-citation xml:lang="en">Kim JM, Wu H, Green G et al. CD2-associated protein haploinsufficiency is linked to glomerular disease susceptibility. Science 2003; 300 (5623): 1298-1300. Doi: 10.1126/science.1081068</mixed-citation></citation-alternatives></ref><ref id="cit141"><label>141</label><citation-alternatives><mixed-citation xml:lang="ru">Lowik MM, Groenen PJ, Pronk I et al. Focal segmental glomerulosclerosis in a patient homozygous for a CD2AP mutation. Kidney Int 2007; 72 (10): 1198-1203. Doi: 10.1038/sj.ki.5002469</mixed-citation><mixed-citation xml:lang="en">Lowik MM, Groenen PJ, Pronk I et al. Focal segmental glomerulosclerosis in a patient homozygous for a CD2AP mutation. Kidney Int 2007; 72 (10): 1198-1203. Doi: 10.1038/sj.ki.5002469</mixed-citation></citation-alternatives></ref><ref id="cit142"><label>142</label><citation-alternatives><mixed-citation xml:lang="ru">Gigante M, Pontrelli P, MontemurnoE et al. CD2AP mutations are associated with sporadic nephrotic syndrome and focal segmental glomerulosclerosis (FSGS). Nephrol Dial Transplant 2009; 24 (6): 1858-1864. Doi: 10.1093/ndt/gfn712</mixed-citation><mixed-citation xml:lang="en">Gigante M, Pontrelli P, MontemurnoE et al. CD2AP mutations are associated with sporadic nephrotic syndrome and focal segmental glomerulosclerosis (FSGS). Nephrol Dial Transplant 2009; 24 (6): 1858-1864. Doi: 10.1093/ndt/gfn712</mixed-citation></citation-alternatives></ref><ref id="cit143"><label>143</label><citation-alternatives><mixed-citation xml:lang="ru">Shih NY, Li J, Karpitskii V et al. Congenital nephrotic syndrome in mice lacking CD2-associated protein. Science 1999; 286: (5438): 312-315</mixed-citation><mixed-citation xml:lang="en">Shih NY, Li J, Karpitskii V et al. Congenital nephrotic syndrome in mice lacking CD2-associated protein. Science 1999; 286: (5438): 312-315</mixed-citation></citation-alternatives></ref><ref id="cit144"><label>144</label><citation-alternatives><mixed-citation xml:lang="ru">Weins A, Kenlan P, Herbert S et al. Mutational and biological analysis of alpha-actinin-4 in focal segmental glomerulosclerosis. J Am Soc Nephrol 2005; 16 (12): 3694-3701. Doi: 10.1681/ASN.2005070706</mixed-citation><mixed-citation xml:lang="en">Weins A, Kenlan P, Herbert S et al. Mutational and biological analysis of alpha-actinin-4 in focal segmental glomerulosclerosis. J Am Soc Nephrol 2005; 16 (12): 3694-3701. Doi: 10.1681/ASN.2005070706</mixed-citation></citation-alternatives></ref><ref id="cit145"><label>145</label><citation-alternatives><mixed-citation xml:lang="ru">Kaplan JM, Kim SH, North KN et al. Mutation in ACTN4, encoding alpha-actinin-4, cause familial segmental glomerulosclerosis. Nat Genet 2000; 24 (3): 251-256. Doi: 10.1038/73456</mixed-citation><mixed-citation xml:lang="en">Kaplan JM, Kim SH, North KN et al. Mutation in ACTN4, encoding alpha-actinin-4, cause familial segmental glomerulosclerosis. Nat Genet 2000; 24 (3): 251-256. Doi: 10.1038/73456</mixed-citation></citation-alternatives></ref><ref id="cit146"><label>146</label><citation-alternatives><mixed-citation xml:lang="ru">Frishberg X Rinat Ch, Feinstein S et al. Mutated podocyn manifesting as CMV-associated congenital nephrotic syndrome. Pediatr Nephrol 2003; 18 (3): 273-275. Doi: 10.1007/s00467-003-1079-3</mixed-citation><mixed-citation xml:lang="en">Frishberg X Rinat Ch, Feinstein S et al. Mutated podocyn manifesting as CMV-associated congenital nephrotic syndrome. Pediatr Nephrol 2003; 18 (3): 273-275. Doi: 10.1007/s00467-003-1079-3</mixed-citation></citation-alternatives></ref><ref id="cit147"><label>147</label><citation-alternatives><mixed-citation xml:lang="ru">Smoyer WE, Mundel P, Gupta A, Welsh MJ. Podocyte alpha-actinin induction precedes foot process effacement in experimental nephrotic syndrome. Am J Physiol 1997; 273 (1 Pt2): F150-F157. Doi: 10.1152/ajprenal.1997.273.1.F150</mixed-citation><mixed-citation xml:lang="en">Smoyer WE, Mundel P, Gupta A, Welsh MJ. Podocyte alpha-actinin induction precedes foot process effacement in experimental nephrotic syndrome. Am J Physiol 1997; 273 (1 Pt2): F150-F157. Doi: 10.1152/ajprenal.1997.273.1.F150</mixed-citation></citation-alternatives></ref><ref id="cit148"><label>148</label><citation-alternatives><mixed-citation xml:lang="ru">Michaud JL, Lemieux LI, Dube M et al. Focal and segmental glomerulosclerosis in mice with podocyte-specific expression of mutant alpha-actinin-4. JAm Soc Nephrol 2003; 14 (5): 1200-1211.</mixed-citation><mixed-citation xml:lang="en">Michaud JL, Lemieux LI, Dube M et al. Focal and segmental glomerulosclerosis in mice with podocyte-specific expression of mutant alpha-actinin-4. JAm Soc Nephrol 2003; 14 (5): 1200-1211.</mixed-citation></citation-alternatives></ref><ref id="cit149"><label>149</label><citation-alternatives><mixed-citation xml:lang="ru">Cybulsky AV, Takano T, Papillon J et al. Glomerular epithelial cell injury associated with mutant alpha-actinin-4. Am J Physiol Renal Physiol2009; 297 (4): F987-F995. Doi: 10.1152/ajprenal.00055.2009</mixed-citation><mixed-citation xml:lang="en">Cybulsky AV, Takano T, Papillon J et al. Glomerular epithelial cell injury associated with mutant alpha-actinin-4. Am J Physiol Renal Physiol2009; 297 (4): F987-F995. Doi: 10.1152/ajprenal.00055.2009</mixed-citation></citation-alternatives></ref><ref id="cit150"><label>150</label><citation-alternatives><mixed-citation xml:lang="ru">Bi J, Chase SE, Pellenz CD et al. Myosin 1e is a component of the glomerular slit diaphragm complex that regulates actin reorganization during cell-cell contact formation in podocytes. Am J Physiol Renal Physiol 2013; 305 (4): F532-F544. Doi: 10.1152/ajprenal.00223.2013</mixed-citation><mixed-citation xml:lang="en">Bi J, Chase SE, Pellenz CD et al. Myosin 1e is a component of the glomerular slit diaphragm complex that regulates actin reorganization during cell-cell contact formation in podocytes. Am J Physiol Renal Physiol 2013; 305 (4): F532-F544. Doi: 10.1152/ajprenal.00223.2013</mixed-citation></citation-alternatives></ref><ref id="cit151"><label>151</label><citation-alternatives><mixed-citation xml:lang="ru">Mele C, Iatropoulos P, Donadelli R et al. MYO1E mutations and childhood familial focal segmental glomerulosclerosis. N Engl J Med 2011; 365 (4): 295-306. Doi: 10.1056/NEJMoa1101273</mixed-citation><mixed-citation xml:lang="en">Mele C, Iatropoulos P, Donadelli R et al. MYO1E mutations and childhood familial focal segmental glomerulosclerosis. N Engl J Med 2011; 365 (4): 295-306. Doi: 10.1056/NEJMoa1101273</mixed-citation></citation-alternatives></ref><ref id="cit152"><label>152</label><citation-alternatives><mixed-citation xml:lang="ru">Mao J, Wang D, Mataleena P et al. Myo1e impairment results in actin reorganization, podocyte dysfunction, and proteinuria in zebrafish and cultured podocytes. PLoS One 2013; 8 (8): e72750. Doi: 10.1371/journal.pone.0072750</mixed-citation><mixed-citation xml:lang="en">Mao J, Wang D, Mataleena P et al. Myo1e impairment results in actin reorganization, podocyte dysfunction, and proteinuria in zebrafish and cultured podocytes. PLoS One 2013; 8 (8): e72750. Doi: 10.1371/journal.pone.0072750</mixed-citation></citation-alternatives></ref><ref id="cit153"><label>153</label><citation-alternatives><mixed-citation xml:lang="ru">Graham S, Ding M, Sours-Brothers S et al. Down-regulation of TRPC6 protein expression by high glucose, a possible mechanism for the impaired Ca2+ signaling in glomerular mesangial cells in diabetes. Am J Physiol Renal Physiol 2007; 293 (4): F1381-F1390. Doi:10.1152/ajprenal.00185.2007</mixed-citation><mixed-citation xml:lang="en">Graham S, Ding M, Sours-Brothers S et al. Down-regulation of TRPC6 protein expression by high glucose, a possible mechanism for the impaired Ca2+ signaling in glomerular mesangial cells in diabetes. Am J Physiol Renal Physiol 2007; 293 (4): F1381-F1390. Doi:10.1152/ajprenal.00185.2007</mixed-citation></citation-alternatives></ref><ref id="cit154"><label>154</label><citation-alternatives><mixed-citation xml:lang="ru">Reiser J, Polu KR, Moller CC et al. TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function. Net Genet 2005; 37 (7): 739-744. Doi: 10.1038/ng1592</mixed-citation><mixed-citation xml:lang="en">Reiser J, Polu KR, Moller CC et al. TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function. Net Genet 2005; 37 (7): 739-744. Doi: 10.1038/ng1592</mixed-citation></citation-alternatives></ref><ref id="cit155"><label>155</label><citation-alternatives><mixed-citation xml:lang="ru">Winn MP, Conlon PJ, Lynn KL et al. A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis. Science 2005; 308 (5729): 1801-1804. Doi: 10.1126/science.1106215</mixed-citation><mixed-citation xml:lang="en">Winn MP, Conlon PJ, Lynn KL et al. A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis. Science 2005; 308 (5729): 1801-1804. Doi: 10.1126/science.1106215</mixed-citation></citation-alternatives></ref><ref id="cit156"><label>156</label><citation-alternatives><mixed-citation xml:lang="ru">Jiang L, Ding J, Tsai H et al. Over-expressing transient receptor potential cation channel 6 in podocytes induces cytoskel-eton rearrangement through increases of intracellular Ca2+ and RhoA activation. Exp Biol Med (Maywood) 2011; 236 (2): 184-193. Doi: 10.1258/ebm.2010.010237</mixed-citation><mixed-citation xml:lang="en">Jiang L, Ding J, Tsai H et al. Over-expressing transient receptor potential cation channel 6 in podocytes induces cytoskel-eton rearrangement through increases of intracellular Ca2+ and RhoA activation. Exp Biol Med (Maywood) 2011; 236 (2): 184-193. Doi: 10.1258/ebm.2010.010237</mixed-citation></citation-alternatives></ref><ref id="cit157"><label>157</label><citation-alternatives><mixed-citation xml:lang="ru">Hinkes B, Wiggins RC, Gbadegesin R et al. Positional cloning uncovers mutations in PLCE1 responsible for a nephrotic syndrome variant that may be reversible. Nat Genet 2006; 38 (12): 1397-1405. Doi: 10.1038/ng1918</mixed-citation><mixed-citation xml:lang="en">Hinkes B, Wiggins RC, Gbadegesin R et al. Positional cloning uncovers mutations in PLCE1 responsible for a nephrotic syndrome variant that may be reversible. Nat Genet 2006; 38 (12): 1397-1405. Doi: 10.1038/ng1918</mixed-citation></citation-alternatives></ref><ref id="cit158"><label>158</label><citation-alternatives><mixed-citation xml:lang="ru">Gbadegesin R, Hinkes BG, Hoskins BE et al. Mutations in PLCE1 are a major cause of isolated diffuse mesangial sclerosis (IDMS). Nephrol Dial Transplant 2008; 23 (4): 1291-1297. Doi: 10.1093/ndt/gfm759</mixed-citation><mixed-citation xml:lang="en">Gbadegesin R, Hinkes BG, Hoskins BE et al. Mutations in PLCE1 are a major cause of isolated diffuse mesangial sclerosis (IDMS). Nephrol Dial Transplant 2008; 23 (4): 1291-1297. Doi: 10.1093/ndt/gfm759</mixed-citation></citation-alternatives></ref><ref id="cit159"><label>159</label><citation-alternatives><mixed-citation xml:lang="ru">Zhu L, Jiang R, Aoudjit L et al. Activation of RhoA in podocytes induces focal segmental glomerulosclerosis. JAm Soc Nephrol 2011; 22 (9): 1621-1630. DoM0.1681/ASN.2010111146</mixed-citation><mixed-citation xml:lang="en">Zhu L, Jiang R, Aoudjit L et al. Activation of RhoA in podocytes induces focal segmental glomerulosclerosis. JAm Soc Nephrol 2011; 22 (9): 1621-1630. DoM0.1681/ASN.2010111146</mixed-citation></citation-alternatives></ref><ref id="cit160"><label>160</label><citation-alternatives><mixed-citation xml:lang="ru">Blattner SM, Hodgin JB, Nishio M et al. Divergent functions of the Rho GTPases Rac1 and Cdc42 in podocyte injury. Kidney Int 2013; 84 (5): 920-930. Doi: 10.1038/ki.2013.175</mixed-citation><mixed-citation xml:lang="en">Blattner SM, Hodgin JB, Nishio M et al. Divergent functions of the Rho GTPases Rac1 and Cdc42 in podocyte injury. Kidney Int 2013; 84 (5): 920-930. Doi: 10.1038/ki.2013.175</mixed-citation></citation-alternatives></ref><ref id="cit161"><label>161</label><citation-alternatives><mixed-citation xml:lang="ru">Sun H, Schlondorff J, Higgs HN, Pollak MR. Inverted formin 2 regulates actin dynamics by antagonizing Rho/diaphanous-related formin signaling. J Am Soc Nephrol 2013; 24 (6): 917-929. Doi: 10.1681/ASN.2012080834</mixed-citation><mixed-citation xml:lang="en">Sun H, Schlondorff J, Higgs HN, Pollak MR. Inverted formin 2 regulates actin dynamics by antagonizing Rho/diaphanous-related formin signaling. J Am Soc Nephrol 2013; 24 (6): 917-929. Doi: 10.1681/ASN.2012080834</mixed-citation></citation-alternatives></ref><ref id="cit162"><label>162</label><citation-alternatives><mixed-citation xml:lang="ru">Brown EJ, Schlondorff JS, Becker DJ et al. Mutations in the formin gene INF2 cause focal segmental glomerulosclerosis. Nat Genet 2010; 42 (1): 72-76. Doi: 10.1038/ng.505</mixed-citation><mixed-citation xml:lang="en">Brown EJ, Schlondorff JS, Becker DJ et al. Mutations in the formin gene INF2 cause focal segmental glomerulosclerosis. Nat Genet 2010; 42 (1): 72-76. Doi: 10.1038/ng.505</mixed-citation></citation-alternatives></ref><ref id="cit163"><label>163</label><citation-alternatives><mixed-citation xml:lang="ru">Boyer O, Benoit G, Gribouval O et al. Mutations in INF2 are a major cause of autosomal dominant focal segmental glomerulosclerosis. J Am Soc Nephrol 2011; 22 (2): 239-245. Doi: 10.1681/ASN.2010050518</mixed-citation><mixed-citation xml:lang="en">Boyer O, Benoit G, Gribouval O et al. Mutations in INF2 are a major cause of autosomal dominant focal segmental glomerulosclerosis. J Am Soc Nephrol 2011; 22 (2): 239-245. Doi: 10.1681/ASN.2010050518</mixed-citation></citation-alternatives></ref><ref id="cit164"><label>164</label><citation-alternatives><mixed-citation xml:lang="ru">Barua M, Brown EJ, Charoonratana VT et al. Mutations in the INF2 gene account for a significant proportion of familial but not sporadic focal and segmental glomerulosclerosis. Kidney Int 2013; 83 (2): 316-322. Doi: 10.1038/ki.2012.349</mixed-citation><mixed-citation xml:lang="en">Barua M, Brown EJ, Charoonratana VT et al. Mutations in the INF2 gene account for a significant proportion of familial but not sporadic focal and segmental glomerulosclerosis. Kidney Int 2013; 83 (2): 316-322. Doi: 10.1038/ki.2012.349</mixed-citation></citation-alternatives></ref><ref id="cit165"><label>165</label><citation-alternatives><mixed-citation xml:lang="ru">Gbadegesin RA, Lavin PJ, Hall G et al. Inverted formin 2 mutations with variable expression in patients with sporadic and hereditary focal and segmental glomerulosclerosis. Kidney Int 2012; 81 (1): 94-99. Doi: 10.1038/ki.2011.297</mixed-citation><mixed-citation xml:lang="en">Gbadegesin RA, Lavin PJ, Hall G et al. Inverted formin 2 mutations with variable expression in patients with sporadic and hereditary focal and segmental glomerulosclerosis. Kidney Int 2012; 81 (1): 94-99. Doi: 10.1038/ki.2011.297</mixed-citation></citation-alternatives></ref><ref id="cit166"><label>166</label><citation-alternatives><mixed-citation xml:lang="ru">Gee HX Saisawat P, Ashraf S et al. ARHGDIA mutations cause nephrotic syndrome via defective RHO GTPase signaling. J Clin Invest 2013; 123 (8): 3243-3253. Doi: 10.1172/JCI69134</mixed-citation><mixed-citation xml:lang="en">Gee HX Saisawat P, Ashraf S et al. ARHGDIA mutations cause nephrotic syndrome via defective RHO GTPase signaling. J Clin Invest 2013; 123 (8): 3243-3253. Doi: 10.1172/JCI69134</mixed-citation></citation-alternatives></ref><ref id="cit167"><label>167</label><citation-alternatives><mixed-citation xml:lang="ru">Patek CE, Little MH, Fleming S et al. A zinc finger truncation of murine WT1 results in the characteristic urogenital abnormalities of Denys-Drash syndrome. Proc Natl Acad Sci USA 1999; 96 (6): 2931-2936</mixed-citation><mixed-citation xml:lang="en">Patek CE, Little MH, Fleming S et al. A zinc finger truncation of murine WT1 results in the characteristic urogenital abnormalities of Denys-Drash syndrome. Proc Natl Acad Sci USA 1999; 96 (6): 2931-2936</mixed-citation></citation-alternatives></ref><ref id="cit168"><label>168</label><citation-alternatives><mixed-citation xml:lang="ru">Pollak MR. Familial FSGS. Adv Chronic Kidney Dis 2014; 21 (5): 422-425. Doi: 10.1053/j.ackd.2014.06.001</mixed-citation><mixed-citation xml:lang="en">Pollak MR. Familial FSGS. Adv Chronic Kidney Dis 2014; 21 (5): 422-425. Doi: 10.1053/j.ackd.2014.06.001</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
