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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">10.36485/1561-6274-2020-24-2-42-51</article-id><article-id custom-type="elpub" pub-id-type="custom">nefr-1799</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>ОБЗОРЫ И ЛЕКЦИИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS AND LECTURES</subject></subj-group></article-categories><title-group><article-title>Гиперкальциемия у детей</article-title><trans-title-group xml:lang="en"><trans-title>Hypercalcemia in children</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6459-2795</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Папиж</surname><given-names>С. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Papizh</surname><given-names>S. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Папиж Светлана Валентиновна, канд. мед. наук.</p><p>Обособленное структурное подразделение «Научно-исследовательский клинический институт педиатрии имени академика Ю.Е. Вельтищева», отдел наследственных и приобретенных болезней почек, старший научный сотрудник.</p><p>125412, Москва, ул. Талдомская, д. 2.Тел.: +7(495)4832192 </p></bio><bio xml:lang="en"><p>Svetlana V. Papizh MD, PhD.</p><p>Research and Clinical Institute for Pediatrics at the Pirogov Russian National Research Medical University, Department of hereditary and acquired diseases of the kidneys.</p><p>125412,Moscow, Taldomskaya st., 2Phone: +7(495)4832192 </p></bio><email xlink:type="simple">papijsveta@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Российский национальный исследовательский медицинский университет имени Н.И. Пирогова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Russian National Research Medical University named after N.I. Pirogov</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2020</year></pub-date><pub-date pub-type="epub"><day>08</day><month>02</month><year>2020</year></pub-date><volume>24</volume><issue>2</issue><fpage>42</fpage><lpage>51</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Папиж С.В., 2020</copyright-statement><copyright-year>2020</copyright-year><copyright-holder xml:lang="ru">Папиж С.В.</copyright-holder><copyright-holder xml:lang="en">Papizh S.V.</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/1799">https://journal.nephrolog.ru/jour/article/view/1799</self-uri><abstract><p>Гиперкальциемия является проявлением широкого спектра наследственных и приобретенных состояний, встречающихся в терапевтической и педиатрической практике. Кальций участвует в ключевых физиологических процессах, системе коагуляции, метаболизме костной ткани. Кишечная абсорбция и элиминация кальция, его канальцевая реабсорбция и экскреция, ремоделирование костной ткани, а также регулирующее влияние паратгормона и активных форм витамина D являются основой гомеостаза кальция в организме человека. Злокачественные новообразования и первичный гиперпаратиреоз в 80–90 % случаев являются причиной гиперкальциемии у взрослых, тогда как генетические заболевания с нарушением кальций/фосфорного обмена и ятрогенные факторы превалируют в перечне причин гиперкальциемии у новорожденных и детей раннего возраста. Клинические проявления гиперкальциемии у детей неспецифичны вследствие поражения различных органов и систем и зависят от степени повышения уровня кальция крови. Умеренная гиперкальциемия протекает бессимптомно и может быть случайной биохимической находкой. Выраженная и критическая гиперкальциемия сопряжена с высоким риском летальных исходов вследствие нарушения ритма сердца, тяжелой неврологической симптоматики с развитием коматозных состояний. Дифференциально-диагностическое значение имеет определение уровня паратгормона, что позволяет выделить две основные группы заболеваний, протекающих с гиперкальциемией: ПТГ-зависимые и ПТГ-независимые. Верификация первопричин развития гиперкальциемии способствует своевременному устранению триггерных факторов, назначению патогенетической и симптоматической терапии, коррекции питания и образа жизни. В статье освещены основы гомеостаза кальция, клинические проявления, дифференциальнодиагностические алгоритмы и принципы терапии гиперкальциемии у детей.</p></abstract><trans-abstract xml:lang="en"><p>Hypercalcemia is a result of a wide range of hereditary and acquired conditions encountered by general physicians and pediatricians. Calcium participates in several key physiological functions, control of blood coagulation, bone calcification. Calcium homeostasis is tightly regulated by the interplay between absorption from the small intestine and renal tubular reabsorption, bone remodeling, and disposal through the gut and the kidney. These processes are regulated by local and circulating factors. The two main hormones influencing the homeostasis of calcium are PTH and calcitriol. Cancer-associated hypercalcemia and primary hyperparathyroidism are the most frequent causes of hypercalcemia in adults. In neonates and infants, one should look first at genetic and iatrogenic etiologies. The clinical manifestations of hypercalcemia in children are nonspecific due to damage to various organs and systems and depend on the degree of blood calcium level. Mild hypercalcemia is asymptomatic and often discovered during routine blood work. Moderate and severe hypercalcemia may cause cardiac arrhythmias, affect the nervous system. The differential diagnosis of the possible etiologies of hypercalcemia should start with the assessment of serum parathyroid hormone (PTH) concentration. The causes of hypercalcemia can be divided between PTH-mediated and non-PTH-mediated. Identification of the main causes of hypercalcemia contributes to the timely elimination of trigger factors, beginning of treatment, correction of nutrition and lifestyle. The article highlights physiological mechanisms of calcium homeostasis, clinical manifestations, diagnostic algorithms and treatment of hypercalcemia in children.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>гиперкальциемия</kwd><kwd>витамин D</kwd><kwd>паратгормон</kwd><kwd>CYP24A1</kwd><kwd>SLC34A1</kwd><kwd>SLC34A3</kwd><kwd>дети</kwd></kwd-group><kwd-group xml:lang="en"><kwd>hypercalcemia</kwd><kwd>vitamin D</kwd><kwd>parathyroid hormone</kwd><kwd>CYP24A1</kwd><kwd>SLC34A1</kwd><kwd>SLC34A3</kwd><kwd>children</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">Lee CT, Yang CC, Lam KK et al. Hypercalcemia in the emergency department. Am J Med Sci 2006;331:119–123. doi: 10.1097/00000441-200603000-00002</mixed-citation><mixed-citation xml:lang="en">Lee CT, Yang CC, Lam KK et al. Hypercalcemia in the emergency department. 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