<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE root>
<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="review-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Consilium Medicum</journal-id><journal-title-group><journal-title xml:lang="en">Consilium Medicum</journal-title><trans-title-group xml:lang="ru"><trans-title>Consilium Medicum</trans-title></trans-title-group><trans-title-group xml:lang="zh"><trans-title>Consilium Medicum</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2075-1753</issn><issn publication-format="electronic">2542-2170</issn><publisher><publisher-name xml:lang="en">Consilium Medicum</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">706345</article-id><article-id pub-id-type="doi">10.26442/20751753.2026.4.203675</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Articles</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Статьи</subject></subj-group><subj-group subj-group-type="article-type"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Asymptomatic hyperuricemia: rationale for intervention prior to symptom onset. A review</article-title><trans-title-group xml:lang="ru"><trans-title>Бессимптомная гиперурикемия: зачем воздействовать на мишень до появления симптомов?</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9007-4123</contrib-id><contrib-id contrib-id-type="spin">3700-9150</contrib-id><name-alternatives><name xml:lang="en"><surname>Biryukova</surname><given-names>Elena V.</given-names></name><name xml:lang="ru"><surname>Бирюкова</surname><given-names>Елена Валерьевна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>D. Sci. (Med.)</p></bio><bio xml:lang="ru"><p>д-р мед. наук, проф. каф. эндокринологии и диабетологии; врач-эндокринолог</p></bio><email>lena@obsudim.ru</email><xref ref-type="aff" rid="aff1"/><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6388-1544</contrib-id><contrib-id contrib-id-type="spin">4053-3033</contrib-id><name-alternatives><name xml:lang="en"><surname>Platonova</surname><given-names>Nadezhda M.</given-names></name><name xml:lang="ru"><surname>Платонова</surname><given-names>Надежда Михайловна</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>D. Sci. (Med.)</p></bio><bio xml:lang="ru"><p>д-р мед. наук, зав. отд. терапевтической эндокринологии</p></bio><email>lena@obsudim.ru</email><xref ref-type="aff" rid="aff3"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-1548-1487</contrib-id><contrib-id contrib-id-type="spin">2684-1579</contrib-id><name-alternatives><name xml:lang="en"><surname>Shinkin</surname><given-names>Mikhail V.</given-names></name><name xml:lang="ru"><surname>Шинкин</surname><given-names>Михаил Викторович</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>Res.</p></bio><bio xml:lang="ru"><p>науч. сотр. отд. эндокринных и метаболических заболеваний, врач-эндокринолог</p></bio><email>lena@obsudim.ru</email><xref ref-type="aff" rid="aff2"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Russian University of Medicine</institution></aff><aff><institution xml:lang="ru">ФГБОУ ВО «Российский университет медицины» Минздрава России</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">Loginov Moscow Clinical Scientific Center</institution></aff><aff><institution xml:lang="ru">ГБУЗ «Московский клинический научно-практический центр им. А.С. Логинова» Департамента здравоохранения г. Москвы</institution></aff></aff-alternatives><aff-alternatives id="aff3"><aff><institution xml:lang="en">Endocrinology Research Centre</institution></aff><aff><institution xml:lang="ru">ФГБУ «Национальный медицинский исследовательский центр эндокринологии им. акад. И.И. Дедова» Минздрава России</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2026-05-31" publication-format="electronic"><day>31</day><month>05</month><year>2026</year></pub-date><volume>28</volume><issue>4</issue><issue-title xml:lang="en">Endocrinology</issue-title><issue-title xml:lang="ru">Эндокринология</issue-title><fpage>233</fpage><lpage>239</lpage><history><date date-type="received" iso-8601-date="2026-04-17"><day>17</day><month>04</month><year>2026</year></date><date date-type="accepted" iso-8601-date="2026-04-17"><day>17</day><month>04</month><year>2026</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2026, Consilium Medicum</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2026, ООО "Консилиум Медикум"</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="en">Consilium Medicum</copyright-holder><copyright-holder xml:lang="ru">ООО "Консилиум Медикум"</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by-nc-sa/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://consilium.orscience.ru/2075-1753/article/view/706345">https://consilium.orscience.ru/2075-1753/article/view/706345</self-uri><abstract xml:lang="en"><p>In recent decades, the prevalence of hyperuricemia (HU) has more than doubled, presenting a spectrum that ranges from asymptomatic uric acid (UA) elevations to clinically evident gout. HU is often detected during primary screenings of patients diagnosed with obesity, type 2 diabetes mellitus, metabolic syndrome, hypertension, chronic kidney disease, chronic heart failure, and non-alcoholic fatty liver disease. Notably, increased UA concentration significantly contributes to the development of polymorbid conditions and is a critical factor in cardiovascular mortality. This article examines the pathogenic role and prognostic implications of HU in the context of a systemic cascade of cardiometabolic and renal disorders, underscoring the necessity of early prevention and therapeutic strategies to mitigate the risk of complications. Key risk factors associated with HU are analyzed, revealing a strong correlation with age, male sex, and dietary habits. The discussion emphasizes the intricate mechanisms that regulate UA homeostasis, in which the dynamic equilibrium between endogenous synthesis and excretion determines serum UA levels. Noteworthy in this regulatory process are the transporter proteins (URAT1, GLUT9, ABCG2) involved in renal and intestinal excretion pathways. Additionally, serum UA concentrations are correlated with glomerular filtration rates. The growing body of evidence indicating the independent detrimental effects of UA on targeted organs warrants a transition from passive monitoring to an active therapeutic approach. This paper provides an analysis of data supporting the need for early, individualized management of HU, including both non-pharmacological and pharmacological interventions. Special attention is given to medications exhibiting pleiotropic hypouricemic effects. In particular, the use of sodium-glucose cotransporter type 2 inhibitors in patients with type 2 diabetes mellitus, chronic kidney disease, and chronic heart failure is deemed pathogenetically justified within a comprehensive treatment strategy that simultaneously addresses the underlying condition and effectively lowers UA levels. Such a personalized strategy allows achieving a synergistic effect: controlling the underlying disease while effectively reducing UA levels, thereby improving long-term prognosis.</p></abstract><trans-abstract xml:lang="ru"><p>За последние два десятилетия распространенность гиперурикемии (ГУ) увеличилась более чем вдвое. Данное состояние варьируется от бессимптомного повышения уровня мочевой кислоты (МК) до манифестных форм, таких как подагра. ГУ часто выявляется при первичном скрининге у пациентов с ожирением, сахарным диабетом 2-го типа, метаболическим синдромом, артериальной гипертензией, хронической болезнью почек, хронической сердечной недостаточностью, неалкогольной жировой болезнью печени. Повышение концентрации МК выступает значимым фактором формирования полиморбидной патологии и существенным фактором сердечно-сосудистой смертности. В статье рассматриваются патогенетическая роль и прогностическая значимость ГУ в развитии системного каскада кардиометаболических и ренальных нарушений; обосновывается важность стратегий ранней профилактики и лечения для снижения риска осложнений. Работа анализирует ключевые факторы риска: выявлено, что распространенность ГУ тесно коррелирует с возрастом, мужским полом и характером питания. Отдельное внимание авторы уделяют сложным механизмам регуляции гомеостаза МК. Ее концентрация в сыворотке определяется динамическим равновесием между эндогенным синтезом и экскрецией. Особое значение в этом процессе имеет система белков-транспортеров (URAT1, GLUT9, ABCG2), контролирующих почечный и кишечный путь выведения. Уровень МК в сыворотке крови коррелирует со скоростью клубочковой фильтрации. Растущий объем доказательств независимого повреждающего влияния МК на органы-мишени диктует переход от пассивного наблюдения к активной терапевтической тактике. В работе представлен анализ данных, подтверждающих необходимость ранней и индивидуализированной коррекции ГУ, рассматриваются немедикаментозные и фармакологические вмешательства. Особый интерес представляют препараты с плейотропным гипоурикемическим эффектом. Так, применение ингибиторов натрий-глюкозного котранспортера 2-го типа у пациентов с сахарным диабетом 2-го типа, хронической болезнью почек, хронической сердечной недостаточностью патогенетически оправдано в рамках многоцелевой стратегии, позволяющей одновременно контролировать основное заболевание и эффективно корректировать сопутствующую ГУ. Такая персонализированная стратегия позволяет достичь синергетического эффекта: обеспечивать контроль основного заболевания и одновременно эффективно снижать уровень МК, улучшая долгосрочный прогноз.</p></trans-abstract><kwd-group xml:lang="en"><kwd>uric acid</kwd><kwd>hyperuricemia</kwd><kwd>obesity</kwd><kwd>diabetes mellitus type 2</kwd><kwd>chronic kidney disease</kwd><kwd>heart failure</kwd><kwd>sodium-glucose transporter 2 inhibitors</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>мочевая кислота</kwd><kwd>гиперурикемия</kwd><kwd>ожирение</kwd><kwd>сахарный диабет 2-го типа</kwd><kwd>хроническая болезнь почек</kwd><kwd>сердечная недостаточность</kwd><kwd>ингибиторы натрий-глюкозного котранспортера 2-го типа</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Neagu P, Niculae A, Checherita IA. Uric Acid and Oxidative Stress-Relationship with Cardiovascular, Metabolic, and Renal Impairment. Int J Mol Sci. 2022;23(6):3188. DOI:10.3390/ijms23063188</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Елисеева М.Е., Елисеев М.С. Значение гиперурикемии в развитии заболеваний человека и методы ее коррекции. Доктор.Ру. 2019;2(157):47-54 [Eliseeva ME, Eliseev MS. Znachenie giperurikemii v razvitii zabolevanii cheloveka i metody ee korrektsii. Doktor.Ru. 2019;2(157):47-54 (in Russian)]. DOI:10.31550/1727-2378-2019-157-2-47-54</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Ngandeu-Singwe M, Nkeck R, Hamroun A, et al. Worldwide trends in hyperuricaemia from 2000 to 2023: a systematic review and modelling analysis. Lancet Rheumatol. 2026;8(5):e346-e362. DOI:10.1016/S2665-9913(25)00344-3</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Шальнова С.А., Деев А.Д., Артамонова Г.В., и др. Гиперурикемия и ее корреляты в Российской популяции (результаты эпидемиологического исследования ЭССЕ-РФ). Рациональная Фармакотерапия в Кардиологии. 2014;10(2):153-9 [Shalnova SA, Deev AD, Artamonov GV, et al. Hyperuricemia and its correlates in the Russian population (results of ESSE-RF epidemiological study). Ration Pharmacother Cardiol. 2014;10(1):153-9 (in Russian)]. DOI:10.20996/1819-6446-2014-10-2-153-159</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Шальнова С.А., Имаева А.Э., Куценко В.А., и др. Гиперурикемия и артериальная гипертония у лиц трудоспособного возраста: результаты популяционного исследования. Кардиоваскулярная терапия и профилактика. 2023;22(9S):3783 [Shalnova SA, Imaeva AE, Kutsenko VA., et al. Hyperuricemia and hypertension in working-age people: results of a population study. Cardiovascular Therapy and Prevention. 2023;22(9S):3783 (in Russian)]. DOI:10.15829/1728-8800-2023-3783</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Dehlin M, Jacobsson L, Roddy E. Global epidemiology of gout: prevalence, incidence, treatment patterns and risk factors. Nat Rev Rheumatol. 2020;16:380-90. DOI:10.1038/s41584-020-0441-1</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Блинова Н.В., Трушина О.Ю., Кисляк О.А., и др. Консенсус по ведению пациентов с гиперурикемией и высоким сердечно-сосудистым риском: 2025. Системные гипертензии. 2025;(2):5-17 [Blinova NV, Trushina OI, Kislyak OA, et al. Consensus on the management of patients with hyperuricemia and high cardiovascular risk: 2025. Systemic Hypertension. 2025;22(2):5-17 (in Russian)]. DOI:10.38109/2075-082X-2025-2-5-17</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Timsans J, Palomäki A, Kauppi M. Gout and Hyperuricemia: A Narrative Review of Their Comorbidities and Clinical Implications. J Clin Med. 2024;13(24):7616. DOI:10.3390/jcm13247616</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>Du L, Zong Y, Li H, Wang. Q. Hyperuricemia and its related diseases: mechanisms and advances in therapy. Signal Transduct Target Ther. 2024;9(1):212. DOI:10.1038/s41392-024-01916-y</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Huang H, Huang B, Li Y, et al. Uric acid and risk of heart failure: a systematic review and meta-analysis. Eur J Heart Fail. 2014;16(1):15-24. DOI:10.1093/eurjhf/hft132</mixed-citation></ref><ref id="B11"><label>11.</label><mixed-citation>Zhu Y, Pandya BJ, Choi HK. Comorbidities of gout and hyperuricemia in the US general population: NHANES 2007–2008. Am J Med. 2012;125(7):67987.DOI:10.1016/j.amjmed.2011.09.033.</mixed-citation></ref><ref id="B12"><label>12.</label><mixed-citation>Gherghina ME, Peride I, Tiglis M, et al. Uric Acid and Oxidative Stress-Relationship with Cardiovascular, Metabolic, and Renal Impairment. Int J Mol Sci. 2022;23(6):3188. DOI:10.3390/ijms23063188.</mixed-citation></ref><ref id="B13"><label>13.</label><mixed-citation>Novikov A, Fu Y, Huang W, et al. SGLT2 inhibition and renal urate excretion: role of luminal glucose, GLUT9, and URAT1. Am J Physiol Renal Physiol. 2019;316:F173-85. DOI:10.1152/ajprenal.00462.2018</mixed-citation></ref><ref id="B14"><label>14.</label><mixed-citation>Hyndman D, Liu S, Miner JN. Urate handling in the human body. Curr Rheumatol Rep. 2016;18:34.</mixed-citation></ref><ref id="B15"><label>15.</label><mixed-citation>Kim SH, Shin J, Son H-E, Kang D-H. Role of urate transporters in the kidneys and intestine in uric acid homeostasis. Kidney Res Clin Pract. 2025. DOI:10.23876/j.krcp.24.321</mixed-citation></ref><ref id="B16"><label>16.</label><mixed-citation>Barnini C, Russo E, Leoncini G, Ghinatti MG. Asymptomatic Hyperuricemia and the Kidney: Lessons from the URRAH Study. Metabolites. 2025;15(1):11. DOI:10.3390/metabo15010011</mixed-citation></ref><ref id="B17"><label>17.</label><mixed-citation>Chen Y, Zhao Z, Li Y, Li L. Characterizations of the Urate Transporter, GLUT9, and Its Potent Inhibitors by Patch-Clamp Technique. SLAS Discov. 2021;26(3):450-9. DOI:10.1177/2472555220949501</mixed-citation></ref><ref id="B18"><label>18.</label><mixed-citation>Gherghina M-E, Peride I, Tiglis M, et al. Uric Acid and Oxidative Stress-Relationship with Cardiovascular, Metabolic, and Renal Impairment. Int J Mol Sci. 2022;23(6):3188. DOI:10.3390/ijms23063188</mixed-citation></ref><ref id="B19"><label>19.</label><mixed-citation>Takada T, Miyata H, Toyoda Y, Nakayama A. Regulation of Urate Homeostasis by Membrane Transporters. Gout Urate Cryst Depos Dis. 2024;2(2):206-19. DOI:10.3390/gucdd2020016</mixed-citation></ref><ref id="B20"><label>20.</label><mixed-citation>Zapf AM, Woodward OM. SGLT2 Inhibitors and Uric Acid Homeostasis. Gout Urate Cryst Depos Dis. 2024;2(2):157-72. DOI:10.3390/gucdd2020014</mixed-citation></ref><ref id="B21"><label>21.</label><mixed-citation>Lytvyn Y, Škrtić M, Yang GK, et al. Glycosuria-mediated urinary uric acid excretion in patients with uncomplicated type 1 diabetes mellitus. Am J Physiol Renal Physiol. 2015;308:F77-F83. DOI:10.1152/ajprenal.00555.2014</mixed-citation></ref><ref id="B22"><label>22.</label><mixed-citation>Mahadita GW, Suwitra K. The Role of hyperuricemia in the pathogenesis and progressivity of chronic kidney disease. Open Access Macedonian Journal of Medical Sciences. 2021;9(F):428-35. DOI:10.3889/oamjms.2021.7100</mixed-citation></ref><ref id="B23"><label>23.</label><mixed-citation>Wen S, Arakawa H, Tamai I. Uric acid in health and disease: From physiological functions to pathogenic mechanisms. Pharmacol Ther. 2024:256:108615. DOI:10.1016/j.pharmthera.2024.108615</mixed-citation></ref><ref id="B24"><label>24.</label><mixed-citation>Fiori E, De Fazio L, Pidone C, Perone F. Asymptomatic hyperuricemia: to treat or not a threat? A clinical and evidence-based approach to the management of hyperuricemia in the context of cardiovascular diseases. J Hypertens. 2024;42(10):1665-80. DOI:10.1097/HJH.0000000000003807</mixed-citation></ref><ref id="B25"><label>25.</label><mixed-citation>Li Y, Zhao L, Qi, W. Uric acid, as a double-edged sword, affects the activity of epidermal growth factor (EGF) on human umbilical vein endothelial cells by regulating aging process. Bioengineered. 2022;13:3877-95. DOI:10.1080/21655979.2022.2027172</mixed-citation></ref><ref id="B26"><label>26.</label><mixed-citation>Павлова З.Ш., Голодников И.И., Камалов А.А., Низов А.Н. Роль фруктозы в генезе нефролитиаза. Урология. 2019;1:114-8 [Pavlova ZSh, Golodnikov II, Kamalov AA, Nizov AN. Rol fruktozy v geneze nefrolitiaza. Urologia. 2019;1:114-8 (in Russian)]. DOI:10.18565/urology.2019.16.114-118</mixed-citation></ref><ref id="B27"><label>27.</label><mixed-citation>Johnson RJ, Lozada LGS, Lanaspa MA, et al. Uric Acid and Chronic Kidney Disease: Still More to Do. Kidney Int Rep. 2022;8(2):229-39. DOI:10.1016/j.ekir.2022.11.016</mixed-citation></ref><ref id="B28"><label>28.</label><mixed-citation>Bhatnagar V, Richard EL, Wu W, et al. Analysis of ABCG2 and other urate transporters in uric acid homeostasis in chronic kidney disease: potential role of remote sensing and signaling. Clin Kidney J. 2016;9:444-53. DOI:10.1093/ckj/sfw010. 27274832</mixed-citation></ref><ref id="B29"><label>29.</label><mixed-citation>Han Y, Zhang Y, Cao Y, et al. Exploration of the association between serum uric acid and testosterone in adult males: NHANES 2011-2016. Transl Androl Urol. 2021;10:272-82. DOI:10.21037/tau-20-1114. 33532316</mixed-citation></ref><ref id="B30"><label>30.</label><mixed-citation>Schakman O, Gilson H, Thissen JP. Mechanisms of glucocorticoid-induced myopathy. J Endocrinol. 2008;197:1-10. DOI:10.1677/joe-07-0606.18372227</mixed-citation></ref><ref id="B31"><label>31.</label><mixed-citation>Li G, Han L, Ma R, et al. Glucocorticoids increase renal excretion of urate in mice by downregulating urate transporter 1. Drug Metab Dispos. 2019;47:1343-51. DOI:10.1124/dmd.119.087700. 31519697</mixed-citation></ref><ref id="B32"><label>32.</label><mixed-citation>Giordano N, Santacroce C, Mattii G, et al. Hyperuricemia and gout in thyroid endocrine disorders. Clin Exp Rheumatol. 2001;19:661-5.</mixed-citation></ref><ref id="B33"><label>33.</label><mixed-citation>Malagrinò M, Zavatt G. Uric Acid in Primary Hyperparathyroidism: Marker, Consequence, or Bystander? Metabolites. 2025;15(7):444. DOI:10.3390/metabo15070444</mixed-citation></ref><ref id="B34"><label>34.</label><mixed-citation>McCormick N, O’Connor MJ, Yokose C, et al. Assessing the Causal Relationships Between Insulin Resistance and Hyperuricemia and Gout Using Bidirectional Mendelian Randomization. Arthritis Rheumatol. 2021;73:2096-104. DOI:10.1002/art.41779</mixed-citation></ref><ref id="B35"><label>35.</label><mixed-citation>Tsushima Y, Nishizawa H, Tochino Y, et al. Uric acid secretion from adipose tissue and its increase in obesity. J Biol Chem. 2013;288:27138-49. DOI:10.1074/jbc.m113.485094</mixed-citation></ref><ref id="B36"><label>36.</label><mixed-citation>Maloberti A, Tognola C, Garofani I, et al. Uric acid and metabolic syndrome: Importance of hyperuricemia cut-off. Int J Cardiol. 2024;417:132527. DOI:10.1016/j.ijcard.2024.132527</mixed-citation></ref><ref id="B37"><label>37.</label><mixed-citation>Yeo C, Kaushal S, Lim B, et al. Impact of bariatric surgery on serum uric acid levels and the incidence of gout-A meta-analysis. Obes Rev. 2019;20(12):1759-70. DOI:10.1111/obr.12940</mixed-citation></ref><ref id="B38"><label>38.</label><mixed-citation>Perez-Ruiz F, Aniel-Quiroga MA, Herrero-Beites AM, et al. Renal clearance of uric acid is linked to insulin resistance and lower excretion of sodium in gout patients. Rheumatol Int. 2015;35:1519-24. DOI:10.1007/s00296-015-3242-0. 25763991</mixed-citation></ref><ref id="B39"><label>39.</label><mixed-citation>Schunk SJ, Kleber ME, März W, et al. Genetically determined NLRP3 inflammasome activation associates with systemic inflammation and cardiovascular mortality. Eur Heart J. 2021;42(18):1742-56. DOI:10.1093/eurheartj/ehab107</mixed-citation></ref><ref id="B40"><label>40.</label><mixed-citation>Maloberti A, Mengozzi A, Russo E, et al. The results of the URRAH (Uric Acid Right for Heart Health) Project: a focus on hyperuricemia in relation to cardiovascular and kidney disease and its role in metabolic dysregulation. High Blood Press Cardiovasc Prev. 2023;30:411-25. DOI:10.1007/s40292-023-00602-4</mixed-citation></ref><ref id="B41"><label>41.</label><mixed-citation>Masulli M, D’Elia L, Angeli F, et al. Serum uric acid levels threshold for mortality in diabetic individuals: the URic acid right for heArt health (URRAH) project. Nutr Metab Cardiovasc Dis. 2022;32(5):1245-52. DOI:10.1016/j.numecd.2022.01.028</mixed-citation></ref><ref id="B42"><label>42.</label><mixed-citation>Richette P, Poitou C, Manivet P, et al. Weight Loss, Xanthine Oxidase, and Serum Urate Levels: A Prospective Longitudinal Study of Obese Patients. Arthritis Care Res (Hoboken). 2016;68(7):1036-42. DOI:10.1002/acr.22798</mixed-citation></ref><ref id="B43"><label>43.</label><mixed-citation>Chen JH, Wen CP, Wu SB, et al. Attenuating the mortality risk of high serum uric acid: the role of physical activity underused. Ann Rheum Dis. 2015;74(11):2034-42. DOI:10.1136/annrheumdis-2014-205312</mixed-citation></ref><ref id="B44"><label>44.</label><mixed-citation>Hanke J, Romejko K, Niemczyk S. Sodium-Glucose Cotransporter-2 Inhibitors in Diabetes and Beyond: Mechanisms, Pleiotropic Benefits, and Clinical Use-Reviewing Protective Effects Exceeding Glycemic Control. Molecules. 2025;30(20):4125. DOI:10.3390/molecules30204125</mixed-citation></ref><ref id="B45"><label>45.</label><mixed-citation>Stevens PE, Ahmed SB, Carrero JJ, et al. KDIGO 2024 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int. 2024;105:S117-314. DOI:10.1016/j.kint.2023.10.018</mixed-citation></ref><ref id="B46"><label>46.</label><mixed-citation>Kochanowska A, Rusztyn P, Szczerkowska K, et al. Sodium–Glucose Cotransporter 2 Inhibitors to Decrease the Uric Acid Concentration – A Novel Mechanism of Action. J Cardiovasc Dev Dis. 2023;10:268. DOI:10.3390/jcdd10070268</mixed-citation></ref><ref id="B47"><label>47.</label><mixed-citation>Akbari A, Rafiee M, Sathyapalan T, Sahebkar A. Impacts of Sodium/Glucose Cotransporter-2 Inhibitors on Circulating Uric Acid Concentrations: A Systematic Review and Meta-Analysis. J Diabetes Res. 2022;2022:7520632. DOI:10.1155/2022/7520632</mixed-citation></ref><ref id="B48"><label>48.</label><mixed-citation>Yip ASY, Leong S, Teo YH, et al. Effect of sodium-glucose cotransporter-2 (SGLT2) inhibitors on serum urate levels in patients with and without diabetes: a systematic review and meta-regression of 43 randomized controlled trials. Ther Adv Chronic Dis. 2022;13:20406223221083509. DOI:10.1177/20406223221083509</mixed-citation></ref><ref id="B49"><label>49.</label><mixed-citation>Packer M. Hyperuricemia and Gout Reduction by SGLT2 Inhibitors in Diabetes and Heart Failure: JACC Review Topic of the Week. J Am Coll Cardiol. 2024;83(2):371-81. DOI:10.1016/j.jacc.2023.10.030</mixed-citation></ref><ref id="B50"><label>50.</label><mixed-citation>Umino H, Hasegawa K, Minakuchi H, et al. High basolateral glucose increases sodium-glucose cotransporter 2 and reduces sirtuin-1 in renal tubules through glucose transporter-2 detection. Sci Rep. 2018;8:6791. DOI:10.1038/s41598-018-25054-y</mixed-citation></ref><ref id="B51"><label>51.</label><mixed-citation>Diallo A, Diallo MF, Carlos-Bolumbu M, Galtier F. Uric acid-lowering effects of sodium-glucose cotransporter 2 inhibitors for preventing cardiovascular events and mortality: A systematic review and meta-analysis. Diabetes Obes Metab. 2024;26(5):1980-5. DOI:10.1111/dom.15483</mixed-citation></ref><ref id="B52"><label>52.</label><mixed-citation>Hu X, Yang Y, Hu X, et al. Effects of sodium-glucose cotransporter 2 inhibitors on serum uric acid in patients with type 2 diabetes mellitus: A systematic review and network meta-analysis. Diabetes Obes Metab. 2022;24(2):228-38. DOI:10.1111/dom.14570</mixed-citation></ref><ref id="B53"><label>53.</label><mixed-citation>Yang S, Hu Q, Kexin Liu K, et al. Serum uric acid reduction through SGLT2 inhibitors: evidence from a systematic review and meta-analysis. Front Pharmacol. 2025:16:1551390. DOI:10.3389/fphar.2025.1551390</mixed-citation></ref><ref id="B54"><label>54.</label><mixed-citation>Алгоритмы специализированной медицинской помощи больных сахарным диабетом. Под ред. И.И. Дедова, М.В. Шестаковой, О.Ю. Сухаревой. 12-й вып. Сахарный диабет. 2025;28(5S): 1-175 [Standards of Specialized Diabetes Care. Edited by II Dedov, MV Shestakova, OYu Sukhareva. 12th Ed. Diabetes mellitus. 2025;28(5S):1-175 (in Russian)].</mixed-citation></ref></ref-list></back></article>
