References

medsovet

Медицинский Совет

Meditsinskiy sovet = Medical Council

2079-701X2658-5790

REMEDIUM GROUP Ltd.

10.21518/2079-701X-2017-20-151-156

medsovet-2246

Research Article

Эндокринология

Endocrinology

ДИАГНОСТИКА И ЛЕЧЕНИЕ ПАЦИЕНТОВ С ВТОРИЧНЫМ ГИПЕРПАРАТИРЕОЗОМ И ПОЧЕЧНОЙ НЕДОСТАТОЧНОСТЬЮ ВОЗМОЖНОСТИ ПРИМЕНЕНИЯ ПАРИКАЛЬЦИТОЛА

DIAGNOSIS AND TREATMENT OF PATIENTS WITH SECONDARY HYPERPARATHYROIDISM AND RENAL INSUFFICIENCY. THERAPEUTIC POTENTIAL OF PARICALCITOL

Белая

Ж. Е.

Belaya

Zh. E.

доктор медицинских наук, профессор.

Москва.

MD, Prof.

Moscow.

Рожинская

Л. Я.

Rozhinskaya

L. Ya.

доктор медицинских наук, профессор.

Москва.

MD, Prof.

Moscow.

Национальный медицинский исследовательский центр эндокринологии Минздрава России.РоссияNational Medical Research Center of Endocrinology of the Ministry of Health of Russia.Russian Federation

2017

07012018

020151156

2018

Белая Ж.Е., Рожинская Л.Я.

Belaya Z.E., Rozhinskaya L.Y.

Данная работа распространяется под лицензией Creative Commons Attribution 4.0.

This work is licensed under a Creative Commons Attribution 4.0 License.

https://www.med-sovet.pro/jour/article/view/2246

Обзор литературы посвящен проблеме вторичного гиперпаратиреоза (ВГПТ) на фоне хронической болезни почек. Начальные проявления заболевания могут наблюдаться уже при минимальном снижении скорости клубочковой фильтрации и патофизиологически связаны с нарушениями нормального метаболизма витамина D с его превращением в D-гормон. В основе патогенеза ВГПТ лежит депривация D-гормона с запуском патофизиологических механизмов нарушения костного ремоделирования, повышения ФРФ-23, ПТГ, изменениями содержания фосфора и кальция в сыворотке крови, что в последующем приводит к значимым изменениям структуры костной ткани и кардиоваскулярным осложнениям. Активные метаболиты витамина D и аналоги витамина D (парикальцитол) были разработаны для заместительной терапии активными формами витамина D в условиях дефицита D-гормона. Парикальцитол способен в силу своего химического строения и фармакокинетики в большей степени блокировать синтез паратгормона и в меньшей степени усиливать всасывание кальция и фосфора в кишечнике, что дает ему преимущества перед ранее существовавшими активными метаболитами.

A review of the literature is devoted to the issue of secondary hyperparathyroidism (SHPT) with underlying chronic renal failure. Initial manifestations of the disease can be observed even with a minimal decrease in the rate of glomerular filtration and are pathophysiologically associated with violations of normal metabolism of vitamin D with its conversion into D-hormone. SHPT pathogenesis is based on the D-hormone deprivation and triggering of pathophysiology mechanisms of bone remodelling, increased FRP-23, PTH, changes in the serum levels of calcium and phosphorus, which may further lead to significant changes in the bone tissue structure and cardiovascular complications. Active metabolites of vitamin D and vitamin D analogues (Paricalcitol) were developed for the replacement of active forms of vitamin D in conditions of D-hormone deficiency. Due to its chemical structure and pharmacokinetics, Paricalcitol is able to block the synthesis of parathyroid hormone to a greater extent and increase the absorption of calcium and phosphorus in the intestine to a lesser extent, which gives it advantages over pre-existing active metabolites

вторичный гиперпаратиреозпочечная недостаточностьпарикальцитол

secondary hyperparathyroidismrenal failureParicalcitol

References1

Егшатян Л.В., Рожинская Л.Я. Медикаментоз ные методы коррекции почечной остеодист рофии. Остеопороз и остеопатии, 2014, 2: 29-35.

Reichel H, Deibert B, Schmidt-Gayk H, et.al. Calcium metabolism in early chronic renal failure: implication s for the pathogenesis of hyperparathyroidism. Nephrol Dial Transplant, 1991, 6: 162-169.

US Renal Data System:USRDS 2004, Annual Data Report. The National Institutes of Health, National Institute of Diabetes and Didgestive and Kidney Diseases, Bethesda, MD, 2004.

Coresh J, Astor BC, Greene T et al. Prevalence of ch Am.Jronic kidney disease and decreased kidney function in the udult US population. Am J Kidney Dis, 2003, 41(1): 1-12.

Kidney Disease: Improving Global Outcomes(KDIGO) CKD Work Group KDIGO 2012 Clinical Practice Guideline for Evaluation and Manadgement of Chronic Kidney Diseases. Ridney inter., Suppl., 2013, 3: 1-150.

Гребенникова Т.А., Белая Ж.Е., Цориев Т.Т., Рожинская Л.Я., Мельниченко Г.А. Эндокринная функция костной ткани. Остеопороз и остеопатии, 2015, 1: 28-37.

Fucumoto S, Yamashita T. FGF-23 is a hormoneregulating phosphate metabolism – Unique biological characteristics of FGF-23. Bone, 2007, 40(5): 1190-1195.

Martin A, Quarles LD. Evidence for FGF23 involvement in a bone-kidney axis regulating bone mineralization and systemic phosphate and vitamin D homeostasis. Adv Exp Med Biol, 2012, 728: 65-83. doi: 10.1007/978-1-4614-0887-1_4.

Jean G, Terrat JC, Vanel T et al. High levels of serum fibroblast growth factor (FGF)-23 are associated with increased mortality in long haemodialysis patients. Nephrol Dial Transplant, 2009, 24(9): 2792–2796. doi: 10.1093/ndt/ gfp191.

Ильин А.В., Арбузова М.И. Фактор роста фибробластов 23 и белок Klotho в патогенезе вторичного гиперпаратиреоза. Остеопороз и остеопатии, 2013, 2: 27-30.

Fukagawa M, Yokoyama K, Koiwa F, Taniguchi M, Shoji T, Kazama JJ, Komaba H, Ando R, Kakuta T, Fujii H, Nakayama M, Shibagaki Y, Fukomoto S, Fujii N, Hattori M, Ashida A, Iseki K, Shigematsu T, Tsukamoto Y, Tsubakihara Y, Tomo T, Hirakata H, Akizawa T. Therapeutic Apheresis and Dialysis, 2013, 17: 247-288.

Boudville N, Inderjeeth C, Elder CJ, Glendenning P. Association between 25-hydroxyvitamin D, somatic muscle weakness and falls risk in endstage renal failure. Clin Endocrinol, 2010, 73: 299-304.

Fusaro M, D’Angelo A, Scalzo G, et al. Vertebral fractures in dialysis: endocrinological disruption of the bone-kidney axis. J. Endocrinol Invest, 2010, 33: 347-352.

Jadoul M, Albert JM, AkibaT et al. Incidence and risk factors for hip or other bone fractures among hemodialysis patients in the Dialysis Outcomes and Practice Patterns Study. Kidney Int, 2006, 70: 1358–66.

Coco M, Rush H. Increased incidence of hip fractures in dialysis patients with low serum parathyroid hormone. Am J Kidney Dis, 2000, 36: 1115–21.

Stehman-Breen CO, Sherrard DJ, Alem AM et al. Risk factors for hip fracture among patients with end-stage renal disease. Kidney Int, 2000, 58: 2200–5.

Lehmann G,Ott U, Kaemmerer D, Schuetze J, Wolf G. Bone histomorphometry and biochemical markers of bone turnover in patients with chronic kidney disease Stages 3–5. Clin Nephrol, 2008, 70: 296–30.

Ureña P, Bernard-Poenaru O, Ostertag A et al. Bone mineral density, biochemical markers and skeletal fractures in haemodialysis patients. Nephrol Dial Transplant, 2003, 18: 2325–33.

Ott SM. Histomorphometric measurements of bone turnover, mineralization, and volume. Clin J Am Soc Nephrol, 2008, 3(Suppl 3): S151–15.

Brandi L, Egljord M, Olgaard K. Pharmacokinetics of 1.25(OH)D3 and 1(OH)D3 and 1(OH)D3 in normal and uraemic men. Nephrol Dial Translpant, 2002, 17: 829-842.

Brown AJ, Finch J, Slatopolsky E.: Differential effects of 19-nor-1,25-dihydroxyvitamin D2 and 1,25 dihydroxyvitamin D3 on intestinal calcium and phosphorus transport. J. Lab Clin Med., 2002, 139: 279-284.

Llach and Yudd M. Paricalcitol in dialysis patients with calcitriol-resistant secondary hyperparathyroidism. Am J Kidney Dis, 2001, 38(suppl): S45-50.

Coyne D, Charya M, Qiu P, et al. Paricalcitol capsule for the treatment of hyperparathyroidism in stage 3 or 4 CKD. Am J Kidney Dis, 2006, 47: 263-276.

Teng M, Wolf M, Lowri E, et.al. Survival of patients undergoing hemodialysis with paricalcitol or calcitriol therapy. New Engl J Med, 2003, 349: 446-456.

Dobrez D, et al. Nephrol Dial Transplant, 2004, 19: 1174-1181.

Coyne, Charya M, Qui P, et al. Paricalcitol capsule for the treatment of secondary hyperparathyroidism in stages 3 and 4 CKD. Am J. Kidney Dis, 2006, 47: 263-276.

Zoccali C, Curatola G, Panuccio V, Tripepi R, Pizzini P, Versace M, Bolignano D, Cutrupi S, Politi R, Tripepi G, Ghiadoni L, Thadhani R, Mallamaci F. Paricalcitol and endothelial function in chronic kidney disease trial. Hypertension, 2014 Nov, 64(5): 1005-11. doi: 10.1161/HYPERTENSIONAHA.114.03748. Epub 2014 Aug 4.

Joergensen C, Tarnow L, Goetze JP, Rossing P. Vitamin D analogue therapy, cardiovascular risk and kidney function in people with Type 1 diabetes mellitus and diabetic nephropathy: a randomized trial. Diabet Med, 2015 Mar, 32(3): 37481. doi: 10.1111/dme.12606. Epub 2014 Nov 5.

Lundwall K, Jörneskog G, Jacobson SH, Spaak J. Paricalcitol, Microvascular and Endothelial Function in Non-Diabetic Chronic Kidney Disease: A Randomized Trial. Am J Nephrol, 2015, 42(4): 265-73. doi: 10.1159/000441364. Epub 2015 Oct 24.

Donate-Correa J, Henríquez-Palop F, MartínNúñez E, Pérez-Delgado N, Muros-de-Fuentes M, Mora-Fernández C, Navarro-González JF. Effect of Paricalcitol on FGF-23 and Klotho in Kidney Transplant Recipients. Transplantation, 2016 Nov, 100(11): 2432-2438.

Trillini M, Cortinovis M, Ruggenenti P, Reyes Loaeza J, Courville K, Ferrer-Siles C, Prandini S, Gaspari F, Cannata A, Villa A, Perna A, Gotti E, Caruso MR, Martinetti D, Remuzzi G, Perico N. Paricalcitol for secondary hyperparathyroidism in renal transplantation. J Am Soc Nephrol, 2015 May, 26(5): 1205-14. doi: 10.1681/ASN.2013111185.

Menezes FG, Abreu RM, Itria A. Costeffectiveness analysis of paricalcitol versus calcitriol for the treatment of SHPT in dialytic patients from the SUS perspective. J Bras Nefrol, 2016 Jul-Sep, 38(3): 313-319. doi: 10.5935/0101-2800.20160048.

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