Perm Medical JournalPerm Medical Journal0136-14492687-1408Eco-Vector568910.17816/pmj33455-60Research ArticleINFLUENCE OF ALDOSTERONE LEVEL ON SYNOVIAL MEMBRANE MORPHOSTRUCTURE IN RHEUMATOID ARTHRITIS PATIENTSKomarovaE Belbelcom@ua.fmRebrovaO A-15082016334556018112016Copyright © 2016, Komarova E.B., Rebrova O.A.2016Aim. The aim of the study was to state the peculiarities of changes in patients with rheumatoid arthritis (RA) depending on blood ALD. Materials and methods. Thirty four patients with diagnosed RA were divided into two groups depending on blood aldosterone (ALD) level (determined with IEA method): group I included 16 patients with ALD level ≤ 130 pg/ml, group II - 18 patients with ALD level 130 pg/ml. To carry out semiquantitative microdetermination of synovial membrane (SM), patients underwent knee joint arthroscopy followed by biopsy. Results. In patients of group II, it was stated as a result of morphological study that SM tectorial cells proliferation 6 rows occurred by 35 % more often, villous hyperplasia and SM edema - by two times more often versus group I ( p 0,05). Direct correlation between blood ALD level and the following microdetermination indices in RA patients was established: villous hyperplasia with tectorial cells proliferation, formation of lymphoid follicles, mycoid swelling and fibrinoid changes. Conclusions. High ALD level can be considered as proliferative-destructive activity marker in patients with rheumatoid arthritis.Rheumatoid arthritissynovial membranealdosteronemorphologyproliferationРевматоидный артритсиновиальная оболчкаальдостеронморфологияпролиферация[Демина А.Б. Часть III. Ультразвуковое исследование в ревматологической практике. Современная ревматология 2013; 7(4): 74-77.][Драпкина О.М. РААС и фиброз. Гепатокардиальные связи. Русcкий медицинский журнал 2011; 19 (4): 1-6.][Лялина В.В., Шехтер А.Б. Артроскопия и морфология синовитов. М.: Наука 2007; 108.][Раденска-Лоповок С.Г. Ревматические заболевания. Морфологическая диагностика: рук-во для врачей / под ред. Г.В. Франка, Р.М. Балабановой. М.: Практическая медицина 2014; 89.][Сыволап В.В., Лукашенко Л.В., Жеманюк С.П., Герасько М.П., Франскявичен Л.В. Возможности антагонистов альдостерона в лечении больных с острым инфарктом миокарда с элевацией ST без ХСН и постинфарктной ХСН с низкой фракцией выброса. Запорожский медицинский журнал 2015; 6 (93).][Af Klint E., Catrina A.I., Matt P., Neregråd P., Lampa J., Ulfgren A.K., Klareskog L., Lindblad S. Evaluation of arthroscopy and macroscopic scoring. Arthritis Research & Therapy 2009; 11 (3): R81.][Annis M. Marney, Nancy J. Brown. Aldosterone and end-organ damage. Clinical Science 2007; 113(6): 267-278.][Biernacka A., Frangogiannis N.G. Aging and Cardiac Fibrosis. Aging. Dis. 2011; 2 (2): 158-173.][Bunda S., Wang Y., Mitts T.F. Aldosterone stimulates elastogenesis in cardiac fibroblasts via mineralocorticoid receptor-independent action involving the consecutive activation of Galpha13, c-Src, the insulin-like growth factor-I receptor, and phosphatidylinositol 3-kinase. Akt. J. Biol. Chem. 2009; 284(24): 16633-16647.][Catena C., Colussi G, Brosolo G., Iogna-Prat L., Sechi L.A. Aldosterone and aldosterone antagonists in cardiac disease: what is known, what is new. Am. J. Cardiovasc. Dis. 2012; 2(1): 50-57.][Duprez D.A. Role of the renin-angiotensin-aldosterone system in vascular remodeling and inflammation: a clinical review. J. Hypertens. 2006; 24(6): 983-991.][Fiebeler A., Muller D.N., Shagdarsuren E., Luft F.C. Aldosterone, mineralocorticoid receptors, and vascular inflammation. Curr. Opin. Nephrol. Hypertens. 2007; 16(2): 134-142.][Hitchon C.A., El-Gabalawy H.S. The synovium in rheumatoid arthritis. Open Rheumatol. J. 2011; 5: 107-114.][Terada Y., Kuwana H., Kobayashi T., Okado T., Suzuki N., Yoshimoto T., Hirata Y., Sasaki S. Aldosterone-stimulated SGK1 activity mediates profibrotic signaling in the mesangium. J. Am. Soc. Nephrol. 2008; 19 (2): 298-309.]