nidНефрология и диализNephrology and Dialysis1680-44222618-9801Российское диализное общество10.28996/2618-9801-2021-4-461-471nid-45Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESСовременные тенденции коррекции гиперфосфатемии у больных хронической болезнью почек. Обзор литературыCurrent trends in correction of hyperphosphatemia in patients with chronic kidney disease. ReviewЕрмоленкоВ. М.ErmolenkoV. M.nephrology@mail.ruФилатоваН. Н.FilatovaN. N.noemail@neicon.ruФГБОУ ДПО РМАНПО МЗ РФРоссияRussian Medical Academy of Continuous Professional EducationRussian Federation202121062024234461471Copyright © Ермоленко В.М., Филатова Н.Н., 20242024Ермоленко В.М., Филатова Н.Н.Ermolenko V.M., Filatova N.N.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://journal.nephro.ru/jour/article/view/45

Коррекция гиперфосфатемии остается важнейшей нерешенной проблемой лечения больных 4 и, в основном, 5 стадиями ХБП, находящихся на лечении хроническим гемодиализом. Используемые в клинике методы - ограничение потребления фосфора, вариации процедур гемодиализа и применение фосфат-связывающих препаратов в определенной степени снижают уровень неорганического фосфора в сыворотке больных, но в половине случаев не позволяют достичь нормальных значений фосфатемии, что приводит к повышению уровня ПТГ и FGF23, вызывающих широкий спектр осложнений, усугубляя как минерально-костные нарушения, так и внекостную кальцификацию, в том числе коронарных артерий, а FGF23 индуцирует гипертрофию левого желудочка. В последние годы для коррекции гиперфосфатемии стали использовать локальные ингибиторы, действующие на транспортеры фосфора, локализованные в почках и ЖКТ. Na+/H+-противопереносчик, экспрессированный у человека в тонком кишечнике и почках, регулирует в ЖКТ абсорбцию натрия, контролируя волемию и внутриклеточный pH и одновременно обеспечивает парацеллюлярную абсорбцию фосфора. Ингибитор Na+/H+-противопереносчика 3 типа (NHE3) тенапанора гидрохлорид снижает абсорбцию натрия и фосфора, а дополнительными показаниями для его назначения являются артериальная гипертензия, сердечная недостаточность и заболевания кишечника. Панингибитор EOS789 угнетает активность Na/Pi-IIb, Pit-1 и Pit-2, также вовлеченных в абсорбцию фосфора в ЖКТ, хорошо зарекомендовал себя в экспериментальных условиях, однако у испытуемых не индуцировал заметного снижения фракционной абсорбции фосфора. Селективный ингибитор Na/Pi-IIa транспортера PF-06869206 оказывает гипофосфатемический эффект у пациентов с ХБП и нарушенной функцией почек, но c сохраненным диурезом. Важнейшей особенностью практически неабсорбируемых в ЖКТ ингибиторов транспортеров фосфора является безопасность и отсутствие при их применении серьезных побочных реакций, а развивающаяся при лечении тенапанором гидрохлоридом диарея облегчает у больных запоры и его назначают пациентам с синдромом «раздраженного кишечника». Таким образом, ингибиторы локальных транспортеров фосфора в сочетании с фосфат-связывающими препаратами способны улучшить коррекцию гиперфосфатемии. Представленный обзор посвящен новому тренду в коррекции гиперфосфатемии, основанному на ингибировании активности локальных транспортеров.

Correction of hyperphosphatemia remains the most important but unsolved problem in the treatment of patients with chronic kidney disease (CKD) stages 4 and 5 and patients on chronic hemodialysis. Currently, to reduce the level of serum phosphorus used to restrict an intake of dietary phosphorus, variety on the duration and frequency of hemodialysis, and the use of different phosphate binders. However this treatment in half of the cases does not allow reaching normal values of phosphorus in serum, and that leads to an increase in PTH and FGF23 and the development of multiple complications. Recently for correction of hyperphosphatemia local inhibitors of phosphorus transporters, which are localized in humans in the kidneys and gastrointestinal tract have began to be used. The Na+/H+-exchanger regulates the absorption of sodium in the gastrointestinal tract, controls volemia and intracellular pH, and provides paracellular absorption of phosphorus. The inhibitor Na+/H+-exchanger type 3 (NHE3) Tenapanor hydrochloride reduced sodium and phosphorus absorption in the intestine. Additional indications for the prescribing of Tenapanor hydrochloride are hypertension, heart failure, and bowel disease. The pan-phosphate transporter inhibitor EOS789 decreased the activity of Na/Pi-IIb, Pit-1, and Pit-2, which are involved in phosphorus absorption in the intestine and has proven itself well under experimental conditions. The selective inhibitor of the Na/Pi IIa transporter PF-06869206 had a hypophosphatemic effect in patients with CKD and preserved diuresis. The most important specialty of local phosphorus transporter inhibitors is safety and the absence of serious adverse reactions during use. Local inhibitors of phosphate transport in combination with phosphate binders can control hyperphosphatemia in patients with chronic kidney disease. This review is d

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The authors declare that there are no conflicts of interest present.