Katerenchuk I. P., Rustamian S. T.

SECONDARY HYPERPARATHYROIDISM: FEATURES OF COURSE, EFFECT ON CARDIOVASCULAR RISK, AND QUALITY OF LIFE IN PATIENTS WITH CHRONIC KIDNEY DISEASE V STAGE


About the author:

Katerenchuk I. P., Rustamian S. T.

Heading:

LITERATURE REVIEWS

Type of article:

Scentific article

Annotation:

The number of patients with end stage renal disease is growing worldwide. Mortality in patients with end stage renal disease remains 10-20 times higher than that in the general population. Based on different epidemiological data, chronic kidney disease affects on average 10% of the population around the world. This is the result of the aging of the population and the increase of civilization diseases such as diabetes, hypertension or obesity. The focus in recent years has thus shifted to optimising the care of these patients during the phase of chronic kidney disease (CKD), before the onset of end stage renal disease. The secondary hyperparathyroidism of chronic renal failure is a result of many factors which result in chronic stimulation of parathyroid hormone secretion and secondary hyperplasia of the parathyroid glands. Renal hyperparathyroidism (rHPT) is a common complication of chronic kidney disease characterized by elevated parathyroid hormone levels secondary to derangements in the homeostasis of calcium, phosphate, and vitamin D. Patients with rHPT experience increased rates of cardiovascular problems and bone disease. Renal HPT leads to a host of bone and cardiovascular problems that ultimately can cause fractures, decreased quality of life, and an increased risk of death. Calcium supplementation, high calcium dialysis, control of plasma phosphate and judicious use of the vitamin D metabolites can, to a large extent, prevent or control the development of secondary hyperparathyroidism. Subtotal parathyroidectomy or total parathyroidectomy with autotransplantation is indicated in certain cases, sometimes on an emergency basis. Prevention of postoperative hypocalcemia requires careful management. Quality of life (QoL) of hemodialysis patients is a major evaluative marker currently measured, while treatment time is a clinical determinant associated with impaired QоL. Treating chronic kidney failure is related to receiving long-term dialysis therapy by patients. Both hemodialysis and peritoneal dialysis significantly change patients’ lives.

Tags:

chronic kidney disease, secondary hyperparathyroidism, parathyroid hormone, phosphorus-calcium metabolism.

Bibliography:

  1. Kolesnyk MO. Natsionalnyi reiestr khvorykh na khronichnu khvorobu nyrok ta patsiientiv z hostrym poshkodzhenniam nyrok: 2015 rik; Derzhavna ustanova «Instytut nefrolohii NAMN Ukrainy»; hol. red. Kolesnyk MO. K.: 2016; 200 s. [in Ukrainian].
  2. Kolesnyk MO, Saidakova NO, Kozlyuk NI, Nikolaenko SS, Snisar LM. Dostupnist likuvannia metodom hemodializu v Ukraini khvorykh na KhKhN V (2006-2015 rr.) Ukrainskyi zhurnal nefrolohii ta dializu. 2016;4(52):3-12. [in Ukrainian].
  3. Grabner A, Amaral AP, Schramm K, Singh S, Sloan A, Yanucil C, et al. Activation of cardiac fibroblast growth factor receptor 4 causes left ventricular hypertrophy. Cell Metab. 2015;22:1020-32.
  4. Lesovoi VN, Andoneva NM, Valkovskaia TL. Vlyianye vtorychnoho hyperparatyreoza na kaltsyfykatsyiu klapanov serdtsa u bolnykh s khronycheskoi bolezniu pochek V D stadyy. Ukrainskyi zhurnal nefrolohii tadializu. 2017;3:76-80. [in Russian].
  5. Efremova OA, Holovyn AY, Khodykyna YuE. Osobennosty fosforno-kaltsyevoho obmena u bolnykh, nakhodiashchykhsia na lechenyy prohrammnym hemodyalyzom. Nauchnyi rezultat. Medytsyna y farmatsyia. 2016;4(2):24-9. [in Russian].
  6. Effat Afaghi, Ali Tayyebi, Behzad Einollahi. Parathyroid gland function in dialysis patients. Journal of Parathyroid Disease. 2014;2(1):33-7.
  7. Volhyna H, Selezeёv D, Balkarova O. Vnekostnaia kaltsyfykatsyia u patsyentov s khronycheskoi bolezniu pochek. Vrach. 2012;7:2-8. [in Russian].
  8. Baldini V, Mastropasqua M, Francucci СM, Erasmo ED. Cardiovascular disease and osteoporosis. J. Endocrinol Invest. 2010;28(10):69-72.
  9. Tkachenko RP, Hubar OS. Ryzyky khirurhichnoho likuvannia vtorynnoho hiperparatyreozu u khvorykh z khronichnoiu nyrkovoiu nedostatnistiu. Svit medytsyny ta biolohii. 2013;4:60-2. [in Ukrainian].
  10. Parsons J. Parathyroid physiology and the skeleton. The Biochemistry and Physiology of Bone. 2012;4:159-225.
  11. Cunningham J, Locatelli F, Rodriguez M. Secondary hyperparathyroidism: pathogenesis, disease progression, and the rapeuticoptions. Clin J Am Soc Nephrol. 2011;6(4):913-21.
  12. Stack BC, Bimston DN, Bodenner DL, Brett EM, Dralle H, Orloff LA, et al. Postoperative hypoparathyroidism-definitions and management. Endocr Pract. 2015;21:674-85.
  13. Topchii II, Denisenko VP, Kirienko OM, Semenovykh PS, Yakimenko YuS, Mazii VV, ta in. Zviazok stanu miokardu z porushenniamy fosfornokaltsiievoho obminu u khvorykh na diabetychnu nefropatiiu. Ukrainskyi zhurnal nefrolohii ta dializu. 2017;2:27-32. [in Ukrainian].
  14. Yamamoto KT, Robinson-Cohen C, de Oliveira MC, Kostina A, Nettleton JA, Ix JH, et al. Dietary phosphorus isassociated with greater left ventricular mass. Kidney Int. 2013;83:707-14.
  15. Dobronravov VA. Sovremennyi vzghliad na patofyzyolohyiu vtorychnoho hyperparatyreoza: rol faktora rosta fybroblastov 23 y Klotho. Nefrolohyia. 2013;4(15):11-20. [in Russian].
  16. Floege J, Kim J, Ireland E, Chazot C, Drueke T, de Francisco A, et al. Serumi PTH, calcium and phosphate, and the risk of mortality in a European haemodialysis population. Nephrol Dial Transplant. 2011;26(6):1948-55.
  17. Levin A, Bakris GL, Molitch M, Smulders M, Tian J. Prevalence of abnormal serum vitamin d, pth, calcium, and phosphorus in patients with chronic kidney disease: Results of the Study to evaluate early kidney disease. Kidney International. 2007;71:31-8.
  18. Mitra Naseri. Hypoparathyroidism versus hyperparathyroidism in pediatric dialysis patients; a single center study. Journal of Nephropathology. 2017:6(4):282-9.
  19. Arnlov J, Carlsson AC, Sundstrom J, Ingelsson E, Larsson A, Lind L, et al. Higher fibroblast growth factor-23 increases the risk of all-cause and cardiovascular mortality in the community. Kidney Int. 2013;83:160-6.
  20. Goldsmith DJ, Cunningham J. Mineral metabolism and vitamin D in chronic kidney disease-more questions than answers. Nat Rev Nephrol. 2011;7:341-6.
  21. Katerenchuk IP, Sarychev LP, Pustovoit HL, Kostrikova YuA, Yarmola TI. Osoblyvosti vikovykh zmin funktsionalnykh struktur nyrok. Visnyk problem biolohii i medytsyny. 2011;2(1):125-7. [in Ukrainian].
  22.  Kaidashev IP, Borzykh OA. Osnovy herontolohii. Chastyna druha. Navchalnyi posibnyk. Poltava: 2011. s. 6-26. [in Ukrainian].
  23. Adiya S, Damdinsuren K, Dorj C. Severe Secondary Hyperparathyroidism in a Hemodialysis Patient: A Case Report from Mongolia. Blood Purif. 2017;44(1):35-40.
  24. Kanbay M, Nicoleta M, Selcoki Y, Ikizek M, Aydin M, Eryonucu B, et al. Fibroblast growth factor 23 and fetuin A are independent predictors for the coronary artery disease extent in mild chronic kidney disease. Clin. J. Am. Soc. Nephrol. 2010;5:1780-6.
  25. Palmer SC, Hayen A, Macaskill P, Pellegrini F, Craig JC, Elder GJ, et al. Serum levels of phosphorus, parathyroid hormone, and calcium and risks of death and cardiovascular disease in individuals with chronic kidney disease: a systematic review and meta-analysis. JAMA. 2011;305:1119-27.

Publication of the article:

«Bulletin of problems biology and medicine» Issue 3 (152), 2019 year, 23-26 pages, index UDK 616.61-002:616.12-008.331.1

DOI: