• Valentyna Moyseyenko Bogomolets National Medical University, MD, PhD, Professor , Academician of the National Academy of Sciences of Ukraine
  • Taras Medvedyev Bogomolets National Medical University, researcher




phosphorus-calcium metabolism, chronic kidney disease, cardiovascular disorders


Introduction. One of the most frequent and difficult problems arising in the treatment of dialysis patients is the correction of phosphorus-calcium metabolism. In chronic renal failure, all links of phosphorus-calcium metabolism are disrupted. With a decrease in the glomerular filtration rate (GFR) below 60 ml / min / 1.73 m2, the filtration of phosphorus decreases and its concentration in the blood serum increases, which causes an increase in the secretion of parathyroid hormone (PTH).
Goal. To summarize the information about the role of hormonal regulation of phosphorus-calcium metabolism in the pathogenesis of chronic kidney disease and cardiovascular diseases, it is accompanied, and to analyze the main therapeutic approaches for the correction of these disorders.
Materials and methods. Bibliographic - a theoretical analysis is carried out and a generalization of literature data is carried out, the actual content is analyzed. In the study, a questionnaire-survey method was used, as well as description, analysis, abstracting.
Results and discussion. PTH is produced by the main cells of the parathyroid glands (PTH). Serum Ca2+ concentration is the main modulator of PTH secretion [2]. Stimulation of the calcium-sensitive receptors (CSR) of the thyroid gland through a cascade of reactions ultimately leads to the suppression of PTH secretion. An additional stimulus for an increase in PTH secretion is hyperphosphatemia. PTH has the following physiological effects: stimulates the resorption of calcium from bone tissue, reabsorption of calcium in the renal tubules. Vitamin D (D3 and D2), in association with vitamin D-binding protein, is transported to the liver, where it is hydroxylated to form 25 (OH) D or calcidiol (KD), which then undergoes 1α-hydroxylation in the renal tubules, turning into the active form of the vitamin D is calcitriol (KT) or D-hormone. Protein Klotho is a transmembrane protein that, among other effects, provides some degree of insulin sensitivity and slows down the aging process in animal experiments. FGF23 has a phosphaturic effect, stimulates the secretion of PTH and inhibits the 1α-hydroxylase activity of the kidneys, leading to a decrease in the synthesis of QD and its level in the blood serum.
Conclusions. Elevated FGF23 and PTH levels are responsible for the adverse effects of excess phosphate, but inhibition of these compensatory mechanisms is clinically impossible as it leads to dangerous changes in mineral metabolism. At the same time, the prevention of cardiovascular complications in persons with disorders in the FGF23/Klotho system should include correction of the phosphate content, since their atherogenic role has been demonstrated, and attempts to reduce the absorption of phosphates using only phosphate binders can lead to an increase in the absorption of phosphates at a time when phosphate binders are not present in the intestinal cavity. Possibly one therapeutic approach in these patients is dietary control of Ca, P and vitamin D levels with blockade of intestinal active phosphate transport to reduce dietary phosphate absorption.


1. Hu MC, Shi M, Zhang J, Pastor J, Nakatani T, Lanske B, Razzaque MS, Rosenblatt KP, Baum MG, Kuro-o M, Moe OW. Klotho: a novel phosphaturic substance acting as an autocrine enzyme in the renal proximal tubule. FASEB J. 2010; 24:3438–3450. [PubMed: 20466874].
2. Silva BC, Costa AG, Cusano NE, Kousteni S, Bilezikian JP. Catabolic and anabolic actions of parathyroid hormone on the skeleton. J.Endocrinol.Invest. 2011; 34:801–810. [PubMed: 21946081.
3. Razzaque MS, St_Arnaud R, Taguchi T, Lanske B. FGF-23, vitamin D and calcification: the unholy triad. Nephrol Dial Transplant 2005; 20 (10): 2032-2035.
4. Torres PU, Prie D, Beck L et al. Klotho gene, phosphocalcic metabolism, and survival in dialysis. J Ren Nutr 2009; 19 (1): 50-56.
5. Golovin AI, Efremova OA, Khodykina YuE. Features of phosphorus-calcium exchange in patients who are protected by program hemodialysis. Research Result. Medicine and Pharmacy. 2016; 2(4): 24-29.
6. Block G.A., Hulbert-Shearon T.E., Levin N.W., Port F.K. Association of serum phosphorus and calcium x phosphorus product with mortality risk in chronic hemodialysis patients: A national study. Am J Kidney Dis 1998. 31. Pp. 607-617.
7. Wang L., Jerosch-Herold M., Jacobs J. et al. Coronary Artery Calcification and Myocardial Perfusion in Asymptomatic Adults: The MESA
(Multi-Ethnic Study of Atherosclerosis). J. Am. Coll. Cardiol. 2006. 48. Pp. 1018-1026.
8. Никула ТД, Мойсеєнко ВО, Карпенко ОВ. Корекція порушень фосфорно-кальцієвого обміну у хворих на хронічні хвороби нирок.
Видавництво СумДУ, 2011.
9. Craver L., Marco M.P., Martinez I. et al. Mineral metabolism parameters throughout chronic kidney disease stages 1–5-achievement of K/ DOQI target ranges. Nephrol. Dial. Transplant. 2007. 22. Pp. 1171-1176.
10. National Kidney Foundation: Clinical practice guidelines for chronic kidney disease: Evaluation, classification and stratification / Am. J. Kidney Dis. – 2002. – Vol. 39, Suppl. 1. – P. 1-26. 5.
11. Мартинюк Л.П., Мартинюк Л.П., Ружицька О.О. Особливості мінерального обміну та функції паращитоподібних залоз при хронічній хворобі нирок. Журнал «Боль. Суставы. Позвоночник» 2 (06) 2012.
12. Tan AU Jr., Levine B.S., Mazess R.B. et al. Effective suppression of parathyroid hormone by 1 alpha-hydroxy-vitamin D2 in hemodialysis
patients with moderate to severe secondary hyperparathyroidism. Kidney Int. 1997. 51. Pp. 317-323.
13. Danese M., Belozeroff V., Smirnakis K. et al. Consistent control of mineral and bone disorder in incident hemodialysis patients. Clin. J. Am. Soc. Nephrol. 2008. 3. Pp. 1423-1429.
14. Foley, R.N.; Parfrey, P.S.; Harnett, J.D.; Kent, G.M.; Murray, D.C.; Barre P.E. Impact of Hypertension on Cardiomyopathy, Morbidity
and Mortality in End-Stage Renal Disease. Kidney Int. 1996, 49, 1379–1385.
15. London, G.M.; Marchais, S.J.; Guerin, A.P.; Metivier, F.; Pannier, B. Cardiac Hypertrophy and Arterial Alterations in End-Stage Renal Disease: Hemodynamic Factors. Kidney Int. 1993, 43 (suppl. 41), S42–S49.
16. Rodríguez-Ortiz ME, Alcalá-Díaz JF, Canalejo A, Torres-Peña JD, Gómez-Delgado F, Muñoz- Castañeda JR, Delgado-Lista J, Rodríguez
M, López-Miranda J, Almadén Y Fibroblast growth factor 23 predicts carotid atherosclerosis in individuals without kidney disease. The CORDIOPREV study. Eur J Intern Med. 2019 doi: 10.1016/j.ejim.2019.12.008.
17. Suetonia C. Palmer; Andrew Hayen; Petra Macaskill et al. Fabio Pellegrini; Jonathan C. Craig; Grahame J. Elder; Giovanni F. M. Strippoli. 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(11):1119-1127. doi:10.1001/jama.2011.308.
18. Dzgoeva FU, Gatagonova TM, Kadzaeva ZK, Khamitsaeva OV, Kochisova ZKh, Dzutseva AT, Bazaeva BG. Left ventricular hypertrophy in end-stage renal disease and its possible regression as a result of correction of anemia and arterial hypertension. Ter Arkh. 2011; 83(6):42-6.
19. Adeera LevinY.A.N. ChunLi Vitamin D and its analogs: Do they protect against cardiovascular disease in patients with kidney disease? Kidney International Volume 68, Issue 5, November 2005, Pages 1973-1981.



How to Cite

Moyseyenko В., & Medvedyev Т. (2021). HORMONAL REGULATION OF SA-P EXCHANGE IN PATIENTS WITH CHRONIC KIDNEY DISEASE AND THERAPEUTIC APPROACHES TO CORRECTION. Actual Problems of Nephrology, (28), 25–31. https://doi.org/10.37321/nefrology.2021.28-03

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