Secondary Hyperparathyroidism In Chronic Kidney Disease: Mechanism Of Development

  • Yuldasheva N.Kh Department of Internal Medicine No 2 and Endocrinology, Tashkent Medical Academy, Uzbekistan
  • Adilova N.Sh Department of Internal Medicine No 2 and Endocrinology, Tashkent Medical Academy, Uzbekistan
  • Axmedova F.Sh Department of Internal Medicine No 2 and Endocrinology, Tashkent Medical Academy, Uzbekistan
  • Kudratova N.A Department of Internal Medicine No 2 and Endocrinology, Tashkent Medical Academy, Uzbekistan
  • Artikova D.M Department of Internal Medicine No 2 and Endocrinology, Tashkent Medical Academy, Uzbekistan
  • Mirhaydarova F.S. Department of Internal Medicine No 2 and Endocrinology, Tashkent Medical Academy, Uzbekistan
Keywords: Secondary Hyperparathyroidism (SHPT), Chronic Kidney Disease (CKD), Calcium-Phosphorus Metabolism

Abstract

This study explores the mechanisms of secondary hyperparathyroidism (SHPT) development in chronic kidney disease (CKD) and its implications. SHPT arises due to chronic hypocalcemia and is exacerbated by disturbances in calcium-phosphorus metabolism and vitamin D deficiency. A literature review methodology was used, analyzing peer-reviewed studies to understand SHPT's pathophysiology, diagnostic markers, and treatment strategies. Findings indicate that SHPT results in elevated parathyroid hormone (PTH) levels, causing systemic skeletal damage, vascular calcification, and renal osteodystrophy. Early diagnosis involves assessing serum PTH, calcium, and phosphorus levels, alongside imaging and histomorphometric bone analyses. Treatment includes dietary phosphorus restrictions, phosphate binders, vitamin D analogs, calcimimetics, and parathyroidectomy in severe cases. These interventions aim to regulate PTH levels and prevent complications like fractures and calciphylaxis. This research underscores the necessity of a multidisciplinary approach for effective management and highlights the importance of innovative therapies for long-term SHPT control in CKD patients.

References

Silva BC, Bilezikian JP. Parathyroid hormone: anabolic and catabolic actions on the skeleton. Curr Opin Pharmacol. 2015;22:41-50. https://doi.org/10.1016/j.coph.2015.03.005

Civitelli R, Ziambaras K. Calcium and phosphate homeostasis: concerted interplay of new regulators. J Endocrinol Invest. 2011;34:3-7

Isakova T, Nickolas TL, Denburg M, Yarlagadda S, Weiner DE, Gutiérrez OM, Bansal V, Rosas SE, Nigwekar S, Yee J, Kramer H. KDOQI US Commentary on the 2017 KDIGO Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Am J Kidney Dis. 2017 Dec;70(6):737-751

Brown EM, Hebert SC. Calcium-receptor-regulated parathyroid and renal function. Bone. 1997;20:303–9

Slatopolsky E, Finch J, Denda M, et al. Phosphorus restriction prevents parathyroid gland growth. High phosphorus directly stimulates PTH secretion in vitro. J Clin Invest. 1996;97:2534–40

Slatopolsky E, Brown A, Dusso A. Role of phosphorus in the pathogenesis of secondary hyperparathyroidism. Am J Kidney Dis. 2001;37:S54–7. doi: 10.1053/ajkd.2001.20740

Martin KJ, Floege J, Ketteler M. Bone and Mineral Disorders in Chronic Kidney Disease. In: Feehally J, editor. Comprehensive Clinical Nephrology. 6th ed. Springer; Berlin/Heidelberg, Germany: 2019

Chakhtoura MT, Nakhoul NN, Shawwa K, et al. Hypovitaminosis D in bariatric surgery: A systematic review of observational studies. Metabolism. 2016;65(4):574-585. https://doi.org/10.1016/j.metabol.2015.12.004

Johnson M, Maher J, DeMaria E, et al. The Long-term Effects of Gastric Bypass on Vitamin D Metabolism. Ann Surg. 2006;243:701–705

Llach F. Secondary hyperparathyroidism in renal failure: the trade-off hypothesis revisited. Am J Kidney Dis. 1995;25:663–679

Asci G, Ok E, Savas R, et al. The link between bone and coronary calcifications in CKD-5 patients on haemodialysis. Nephrol Dial Transpl. 2011;26:1010-1015

Fang Y, Ginsberg C, Seifert M, et al. CKD-induced wingless/integration1 inhibitors and phosphorus cause the CKD-mineral and bone disorder. J Am Soc Nephrol. 2014;25:1760-1773

Agoro R, White K. Regulation of FGF23 production and phosphate metabolism by bone-kidney interactions. Nat Rev Nephrol. 2023;19(3):185–193

Garcia-Fernandez N, Lavilla J, Martín P, et al. Increased fibroblast growth factor 23 in heart failure: biomarker, mechanism, or both? Am J Hypertens. 2019;32(1):15–17. doi: 10.1093/ajh/hpy153

Ho B, Bergwitz C. FGF23 signalling and physiology. J Mol Endocrinol. 2022;66(2):R23–R32. doi: 10.1530/JME-20-0178

Kuro-O M. Nat Rev Nephrol. The Klotho proteins in health and disease. 2019;15:27–44

Mutation of the mouse klotho gene leads to a syndrome resembling ageing. Kuro-o M, Matsumura Y, Aizawa H, et al. Nature. 1997;390:45–51. doi: 10.1038/36285

In vivo genetic evidence for klotho-dependent, fibroblast growth factor 23 (Fgf23) -mediated regulation of systemic phosphate homeostasis. Nakatani T, Sarraj B, Ohnishi M, et al. FASEB J. 2009;23:433–441. doi: 10.1096/fj.08-114397

Moe S, Drüeke T, Cunningham J, et al. Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2006;69(11):1945-1953. https://doi.org/10.1038/sj.ki.5000414

Moe SM. Renal Osteodystrophy or Kidney-Induced Osteoporosis? Curr Osteoporos Rep. 2017;15(3):194-197. https://doi.org/10.1007/s11914-017-0364-1

Sprague SM, Bellorin-Font E, Jorgetti V, et al. Diagnostic Accuracy of Bone Turnover Markers and Bone Histology in Patients With CKD Treated by Dialysis. Am J Kidney Dis. 2016;67(4):559-566

Okuno S, Inaba M, Ishimura E, et al. Effects of long-term cinacalcet administration on parathyroid gland in hemodialysis patients with secondary hyperparathyroidism. Nephron. 2019;142(2):106-13. doi: 10.1159/000496808

Behets GJ, Spasovski G, Sterling LR, et al. Bone histomorphometry before and after long-term treatment with cinacalcet in dialysis patients with secondary hyperparathyroidism. Kidney Int. 2015;87:846-856. doi: 10.1038/ki.2014.349
Published
2024-12-25
How to Cite
Yuldasheva N.Kh, Adilova N.Sh, Axmedova F.Sh, Kudratova N.A, Artikova D.M, & Mirhaydarova F.S. (2024). Secondary Hyperparathyroidism In Chronic Kidney Disease: Mechanism Of Development. Central Asian Journal of Medical and Natural Science, 6(1), 215-220. Retrieved from https://cajmns.centralasianstudies.org/index.php/CAJMNS/article/view/2688
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Articles