Skip to main content

Advertisement

Log in

Controversies in the Management of Secondary Hyperparathyroidism in Chronic Kidney Disease

  • Kidney and Bone (I Salusky and T Nickolas, Section Editors)
  • Published:
Current Osteoporosis Reports Aims and scope Submit manuscript

Abstract

Secondary hyperparathyroidism is a frequent complication of chronic kidney disease that begins early in the course of renal insufficiency as an adaptive response to maintain mineral homeostasis. This complex disorder affects the bone, leading to an increase in fracture risk and is associated with increased risks of vascular calcification and mortality.

Purpose of Review

In this review, we examine the different strategies available to manage secondary hyperparathyroidism. Particularly, we focus on the adequate control of serum phosphorus by restricting intake and the use of phosphate binders, correction of hypocalcemia while minimizing calcium burden, and reduction in PTH levels through the use of vitamin D sterols and calcimimetics.

Recent Findings

It was observed that although numerous agents directed at the correction of these abnormalities have demonstrated effectiveness on biochemical markers, there is still a relative scarcity of studies demonstrating treatment effectiveness as measured by hard clinical outcomes. In addition, most agents have side effects that may limit their use, even in patients in which the treatment has demonstrated efficacy in controlling these parameters.

Summary

There is still controversy as to what therapeutic regimens to choose for a particular patient and what parameter should be used to follow their effects, including outcomes, side effects, pill burden, and costs, among others. In the present article, we analyze controversial aspects of the different therapeutic agents available. Although many tools and regimens are available, no one by itself is enough for an adequate management of the patient. But rather, combined therapy and individualization of approaches are recommended for better results. We suggest that new studies analyzing the effectiveness of therapeutic approaches to the management of secondary hyperparathyroidism should be directed not only to controlling parathyroid hormone levels but also to the evaluation of long-term outcomes, based on modification of morbidity, mortality, and end organ impact, while reducing side effects and controlling costs, among others.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Fig. 1

Similar content being viewed by others

References

Papers of particular interest, published recently, have been highlighted as: • Of importance

  1. Kidney Disease: Imporoving Global Outcomes (KDIGO) CKD-MBD Word Group. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD). Kidney Int Suppl. 2009(113):S1–130.

  2. 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(11):1119–27.

    CAS  PubMed  Google Scholar 

  3. Martin KJ, Floege J, Ketteler M. Bone and mineral disorders in chronic kidney disease. In: Feehally J, J F, R.J. J, editors. Comprehensive clinical nephrology. Sixth Edition ed2019.

  4. Pereira RC, Juppner H, Azucena-Serrano CE, Yadin O, Salusky IB, Wesseling-Perry K. Patterns of FGF-23, DMP1, and MEPE expression in patients with chronic kidney disease. Bone. 2009;45(6):1161–8.

    CAS  PubMed  PubMed Central  Google Scholar 

  5. Sakan H, Nakatani K, Asai O, Imura A, Tanaka T, Yoshimoto S, et al. Reduced renal alpha-Klotho expression in CKD patients and its effect on renal phosphate handling and vitamin D metabolism. PLoS One. 2014;9(1):e86301.

    PubMed  PubMed Central  Google Scholar 

  6. Smith RC, O'Bryan LM, Farrow EG, Summers LJ, Clinkenbeard EL, Roberts JL, et al. Circulating alphaKlotho influences phosphate handling by controlling FGF23 production. J Clin Invest. 2012;122(12):4710–5.

    CAS  PubMed  PubMed Central  Google Scholar 

  7. KDIGO 2017. Clinical practice guideline update for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD-MBD). Kidney International Supplements. 2017;7(1):1–59.

    Google Scholar 

  8. Blacher J, Guerin AP, Pannier B, Marchais SJ, London GM. Arterial calcifications, arterial stiffness, and cardiovascular risk in end-stage renal disease. Hypertension. 2001;38(4):938–42.

    CAS  PubMed  Google Scholar 

  9. Block GA, Hulbert-Shearon TE, Levin NW, Port FK. Association of serum phosphorus and calcium x phosphate product with mortality risk in chronic hemodialysis patients: a national study. Am J Kidney Dis. 1998;31(4):607–17.

    CAS  PubMed  Google Scholar 

  10. Dhingra R, Sullivan LM, Fox CS, Wang TJ, D'Agostino RB Sr, Gaziano JM, et al. Relations of serum phosphorus and calcium levels to the incidence of cardiovascular disease in the community. Arch Intern Med. 2007;167(9):879–85.

    CAS  PubMed  Google Scholar 

  11. Gutierrez OM, Mannstadt M, Isakova T, Rauh-Hain JA, Tamez H, Shah A, et al. Fibroblast growth factor 23 and mortality among patients undergoing hemodialysis. N Engl J Med. 2008;359(6):584–92.

    CAS  PubMed  PubMed Central  Google Scholar 

  12. Isakova T. Comparison of mineral metabolites as risk factors for adverse clinical outcomes in CKD. Semin Nephrol. 2013;33(2):106–17.

    CAS  PubMed  Google Scholar 

  13. de Fornasari ML, Dos Santos Sens YA. Replacing phosphorus-containing food additives with foods without additives reduces phosphatemia in end-stage renal disease patients: a randomized clinical trial. J Ren Nutr. 2017;27(2):97–105.

    PubMed  Google Scholar 

  14. Nelson SM, Sarabia SR, Christilaw E, Ward EC, Lynch SK, Adams MA, et al. Phosphate-containing prescription medications contribute to the daily phosphate intake in a third of hemodialysis patients. J Ren Nutr. 2017;27(2):91–6.

    CAS  PubMed  Google Scholar 

  15. Elias RM, Alvares VRC, Moyses RMA. Phosphate removal during conventional hemodialysis: a decades-old misconception. Kidney Blood Press Res. 2018;43(1):110–4.

    CAS  PubMed  Google Scholar 

  16. Kjellstrand CM, Ing TS, Kjellstrand PT, Odar-Cederlof I, Lagg CR. Phosphorus dynamics during hemodialysis. Hemodial Int. 2011;15(2):226–33.

    PubMed  Google Scholar 

  17. Kuhlmann MK. Management of hyperphosphatemia. Hemodial Int. 2006;10(4):338–45.

    PubMed  Google Scholar 

  18. Mucsi I, Hercz G, Uldall R, Ouwendyk M, Francoeur R, Pierratos A. Control of serum phosphate without any phosphate binders in patients treated with nocturnal hemodialysis. Kidney Int. 1998;53(5):1399–404.

    CAS  PubMed  Google Scholar 

  19. Sampaio MS, Ruzany F, Dorigo DM, Suassuna JH. Phosphate mass removal during hemodialysis: a comparison between eKT/V-matched conventional and extended dialysis. Am J Nephrol. 2012;36(2):121–6.

    CAS  PubMed  Google Scholar 

  20. Malluche HH. Aluminium and bone disease in chronic renal failure. Nephrol Dial Transplant. 2002;17(Suppl 2):21–4.

    CAS  PubMed  Google Scholar 

  21. Rob PM, Niederstadt C, Reusche E. Dementia in patients undergoing long-term dialysis: aetiology, differential diagnoses, epidemiology and management. CNS Drugs. 2001;15(9):691–9.

    CAS  PubMed  Google Scholar 

  22. Block GA, Wheeler DC, Persky MS, Kestenbaum B, Ketteler M, Spiegel DM, et al. Effects of phosphate binders in moderate CKD. J Am Soc Nephrol. 2012;23(8):1407–15.

    CAS  PubMed  PubMed Central  Google Scholar 

  23. Guerin AP, London GM, Marchais SJ, Metivier F. Arterial stiffening and vascular calcifications in end-stage renal disease. Nephrol Dial Transplant. 2000;15(7):1014–21.

    CAS  PubMed  Google Scholar 

  24. London GM, Guerin AP, Marchais SJ, Metivier F, Pannier B, Adda H. Arterial media calcification in end-stage renal disease: impact on all-cause and cardiovascular mortality. Nephrol Dial Transplant. 2003;18(9):1731–40.

    Google Scholar 

  25. Chertow GM, Burke SK, Raggi P. Treat to goal working G. Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients. Kidney Int. 2002;62(1):245–52.

    CAS  PubMed  Google Scholar 

  26. Block GA, Spiegel DM, Ehrlich J, Mehta R, Lindbergh J, Dreisbach A, et al. Effects of sevelamer and calcium on coronary artery calcification in patients new to hemodialysis. Kidney Int. 2005;68(4):1815–24.

    CAS  PubMed  Google Scholar 

  27. Qunibi W, Moustafa M, Muenz LR, He DY, Kessler PD, Diaz-Buxo JA, et al. A 1-year randomized trial of calcium acetate versus sevelamer on progression of coronary artery calcification in hemodialysis patients with comparable lipid control: the Calcium Acetate Renagel Evaluation-2 (CARE-2) study. Am J Kidney Dis. 2008;51(6):952–65.

    CAS  PubMed  Google Scholar 

  28. Floege J, Kim J, Ireland E, Chazot C, Drueke T, de Francisco A, et al. Serum iPTH, calcium and phosphate, and the risk of mortality in a European haemodialysis population. Nephrol Dial Transplant. 2011;26(6):1948–55.

    CAS  PubMed  Google Scholar 

  29. Suki WN, Zabaneh R, Cangiano JL, Reed J, Fischer D, Garrett L, et al. Effects of sevelamer and calcium-based phosphate binders on mortality in hemodialysis patients. Kidney Int. 2007;72(9):1130–7.

    CAS  PubMed  Google Scholar 

  30. Jamal SA, Vandermeer B, Raggi P, Mendelssohn DC, Chatterley T, Dorgan M, et al. Effect of calcium-based versus non-calcium-based phosphate binders on mortality in patients with chronic kidney disease: an updated systematic review and meta-analysis. Lancet. 2013;382(9900):1268–77.

    CAS  PubMed  Google Scholar 

  31. Patel L, Bernard LM, Elder GJ. Sevelamer versus calcium-based binders for treatment of hyperphosphatemia in CKD: a meta-analysis of randomized controlled trials. Clin J Am Soc Nephrol. 2016;11(2):232–44.

    CAS  PubMed  Google Scholar 

  32. Vervloet MG, van Ballegooijen AJ. Prevention and treatment of hyperphosphatemia in chronic kidney disease. Kidney Int. 2018;93(5):1060–72.

    CAS  PubMed  Google Scholar 

  33. Wald R, Rabbat CG, Girard L, Garg AX, Tennankore K, Tyrwhitt J, et al. Two phosphAte taRGets in end-stage renal disease trial (TARGET): a randomized controlled trial. Clin J Am Soc Nephrol. 2017;12(6):965–73.

    CAS  PubMed  PubMed Central  Google Scholar 

  34. Chertow GM, Burke SK, Dillon MA, Slatopolsky E. Long-term effects of sevelamer hydrochloride on the calcium x phosphate product and lipid profile of haemodialysis patients. Nephrol Dial Transplant. 1999;14(12):2907–14.

    CAS  PubMed  Google Scholar 

  35. Wilkes BM, Reiner D, Kern M, Burke S. Simultaneous lowering of serum phosphate and LDL-cholesterol by sevelamer hydrochloride (RenaGel) in dialysis patients. Clin Nephrol. 1998;50(6):381–6.

    CAS  PubMed  Google Scholar 

  36. Sprague SM. A comparative review of the efficacy and safety of established phosphate binders: calcium, sevelamer, and lanthanum carbonate. Curr Med Res Opin. 2007;23(12):3167–75.

    CAS  PubMed  Google Scholar 

  37. Slatopolsky E, Liapis H, Finch J. Progressive accumulation of lanthanum in the liver of normal and uremic rats. Kidney Int. 2005;68(6):2809–13.

    CAS  PubMed  Google Scholar 

  38. Laville M. Efficacy and safety of lanthanum carbonate in chronic kidney disease patients with hyperphosphataemia. Nephrol Ther. 2011;7(3):154–61.

    CAS  PubMed  Google Scholar 

  39. Ogata H, Fukagawa M, Hirakabata H, Kagimura T. Group atLS. ASN National Meeting: Comparison of lanthanum carbonate and calcium carbonate in the cardiovascular mortality and morbidity in hemofialysis patients; 2018.

    Google Scholar 

  40. • Lewis JB, Sika M, Koury MJ, Chuang P, Schulman G, Smith MT, et al. Ferric citrate controls phosphorus and delivers iron in patients on dialysis. J Am Soc Nephrol. 2015;26(2):493–503. Control of phosphate levels and correction of anemia are important factors in the treatment of CKD patients. This study shows that ferric citrate is an effective phosphate binder, which at the same time increases iron stores, thus reducing the requirements of IV iron and the use of erythropoiesis-stimulating agents to correct anemia. Limitations of the study and of possible use of this type of agent to treat high phosphate levels include patients with high ferritin or TSAT levels as well as those with phosphate > 6.0 as they were not included in the study.

    PubMed  Google Scholar 

  41. • Umanath K, Jalal DI, Greco BA, Umeukeje EM, Reisin E, Manley J, et al. Ferric citrate reduces intravenous iron and erythropoiesis-stimulating agent use in ESRD. J Am Soc Nephrol. 2015;26(10):2578–87. This study adds evidence about the effect of ferric citrate on ferritin levels and transferrin saturation which reduces the requirements for i.v. iron and ESA use in patients with ESRD.

    CAS  PubMed  PubMed Central  Google Scholar 

  42. Cannata-Andia JB, Martin KJ. The challenge of controlling phosphorus in chronic kidney disease. Nephrol Dial Transplant. 2016;31(4):541–7.

    CAS  PubMed  Google Scholar 

  43. Ok E, Asci G, Bayraktaroglu S, Toz H, Ozkahya M, Yilmaz M, et al. Reduction of dialysate calcium level reduces progression of coronary artery calcification and improves low bone turnover in patients on hemodialysis. J Am Soc Nephrol. 2016;27(8):2475–86.

    CAS  PubMed  Google Scholar 

  44. Spasovski G, Gelev S, Masin-Spasovska J, Selim G, Sikole A, Vanholder R. Improvement of bone and mineral parameters related to adynamic bone disease by diminishing dialysate calcium. Bone. 2007;41(4):698–703.

    CAS  PubMed  Google Scholar 

  45. National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis. 2003;42(4 Suppl 3):S1–201.

    Google Scholar 

  46. Kim HW, Kim SH, Kim YO, Jin DC, Song HC, Choi EJ, et al. Impact of dialysate calcium concentration on clinical outcomes in incident hemodialysis patients. Medicine (Baltimore). 2015;94(40):e1694.

    CAS  Google Scholar 

  47. Miller JE, Kovesdy CP, Norris KC, Mehrotra R, Nissenson AR, Kopple JD, et al. Association of cumulatively low or high serum calcium levels with mortality in long-term hemodialysis patients. Am J Nephrol. 2010;32(5):403–13.

    CAS  PubMed  PubMed Central  Google Scholar 

  48. Spiegel DM. Brady K. Kidney Int: Calcium balance in normal individuals and in patients with chronic kidney disease on low- and high-calcium diets; 2012.

    Google Scholar 

  49. Jean G, Chazot C. Individualizing the dialysate calcium concentration. Curr Opin Nephrol Hypertens. 2015;24(6):538–45.

    CAS  PubMed  Google Scholar 

  50. Brown EM, Gamba G, Riccardi D, Lombardi M, Butters R, Kifor O, et al. Cloning and characterization of an extracellular Ca(2+)-sensing receptor from bovine parathyroid. Nature. 1993;366(6455):575–80.

    CAS  PubMed  Google Scholar 

  51. Rodriguez M, Nemeth E, Martin D. The calcium-sensing receptor: a key factor in the pathogenesis of secondary hyperparathyroidism. Am J Physiol Renal Physiol. 2005;288(2):F253–64.

    CAS  PubMed  Google Scholar 

  52. Yano S, Sugimoto T, Tsukamoto T, Chihara K, Kobayashi A, Kitazawa S, et al. Decrease in vitamin D receptor and calcium-sensing receptor in highly proliferative parathyroid adenomas. Eur J Endocrinol. 2003;148(4):403–11.

    CAS  PubMed  Google Scholar 

  53. Sprague SM, Coyne D. Control of secondary hyperparathyroidism by vitamin D receptor agonists in chronic kidney disease. Clin J Am Soc Nephrol. 2010;5(3):512–8.

    CAS  PubMed  Google Scholar 

  54. Batacchi Z, Robinson-Cohen C, Hoofnagle AN, Isakova T, Kestenbaum B, Martin KJ, et al. Effects of vitamin D2 supplementation on vitamin D3 metabolism in health and CKD. Clin J Am Soc Nephrol. 2017;12(9):1498–506.

    CAS  PubMed  PubMed Central  Google Scholar 

  55. Coen G, Mazzaferro S, Bonucci E, Ballanti P, Massimetti C, Donato G, et al. Treatment of secondary hyperparathyroidism of predialysis chronic renal failure with low doses of 1,25(OH)2D3: humoral and histomorphometric results. Miner Electrolyte Metab. 1986;12(5–6):375–82.

    CAS  PubMed  Google Scholar 

  56. Sperschneider H, Humbsch K, Abendroth K. Oral calcitriol pulse therapy in hemodialysis patients. Effects on histomorphometry of bone in renal hyperparathyroidism. Med Klin (Munich). 1997;92(10):597–603.

    CAS  Google Scholar 

  57. Thadhani R, Appelbaum E, Pritchett Y, Chang Y, Wenger J, Tamez H, et al. Vitamin D therapy and cardiac structure and function in patients with chronic kidney disease: the PRIMO randomized controlled trial. JAMA. 2012;307(7):674–84.

    CAS  Google Scholar 

  58. Wang AY, Fang F, Chan J, Wen YY, Qing S, Chan IH, et al. Effect of paricalcitol on left ventricular mass and function in CKD--the OPERA trial. J Am Soc Nephrol. 2014;25(1):175–86.

    CAS  Google Scholar 

  59. Isakova T, Nickolas TL, Denburg M, Yarlagadda S, Weiner DE, Gutierrez OM, et al. 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;70(6):737–51.

    PubMed  Google Scholar 

  60. Harrington PE, Fotsch C. Calcium sensing receptor activators: calcimimetics. Curr Med Chem. 2007;14(28):3027–34.

    CAS  PubMed  Google Scholar 

  61. Block GA, Martin KJ, de Francisco AL, Turner SA, Avram MM, Suranyi MG, et al. Cinacalcet for secondary hyperparathyroidism in patients receiving hemodialysis. N Engl J Med. 2004;350(15):1516–25.

    CAS  PubMed  Google Scholar 

  62. Lindberg JS, Culleton B, Wong G, Borah MF, Clark RV, Shapiro WB, et al. Cinacalcet HCl, an oral calcimimetic agent for the treatment of secondary hyperparathyroidism in hemodialysis and peritoneal dialysis: a randomized, double-blind, multicenter study. J Am Soc Nephrol. 2005;16(3):800–7.

    CAS  PubMed  Google Scholar 

  63. Pereira L, Meng C, Marques D, Frazao JM. Old and new calcimimetics for treatment of secondary hyperparathyroidism: impact on biochemical and relevant clinical outcomes. Clin Kidney J. 2018;11(1):80–8.

    CAS  PubMed  Google Scholar 

  64. Eidman KE, Wetmore JB. Treatment of secondary hyperparathyroidism: how do cinacalcet and etelcalcetide differ? Semin Dial. 2018;31(5):440–4.

    PubMed  Google Scholar 

  65. • Block GA, Bushinsky DA, Cheng S, Cunningham J, Dehmel B, Drueke TB, et al. Effect of etelcalcetide vs cinacalcet on serum parathyroid hormone in patients receiving hemodialysis with secondary hyperparathyroidism: a randomized clinical trial. JAMA. 2017;317(2):156–64. The study shows that both calcimimetics are effective in lowering PTH levels in CKD patients on dialysis with moderate to severe secondary hyperparathyroidism. Etelcalcitide was not inferior to cinacalcet and even demonstrated superiority in lowering PTH, but also was more frequently associated with hypocalcemia. Since the patients included in the study were relatively young, no extrapolation of the results should be done to older patients.

    CAS  PubMed  Google Scholar 

  66. Block GA, Bushinsky DA, Cunningham J, Drueke TB, Ketteler M, Kewalramani R, et al. Effect of etelcalcetide vs placebo on serum parathyroid hormone in patients receiving hemodialysis with secondary hyperparathyroidism: two randomized clinical trials. JAMA. 2017;317(2):146–55.

    CAS  PubMed  Google Scholar 

  67. Pun PH, Abdalla S, Block GA, Chertow GM, Correa-Rotter R, Dehmel B, et al. Cinacalcet, dialysate calcium concentration, and cardiovascular events in the EVOLVE trial. Hemodial Int. 2016;20(3):421–31.

    PubMed  Google Scholar 

  68. Stollenwerk B, Iannazzo S, Cooper K, Belozeroff V. Exploring the potential value of improved care for secondary hyperparathyroidism with a novel calcimimetic therapy. J Med Econ. 2017;20(10):1110–5.

    PubMed  Google Scholar 

  69. Cunningham J, Danese M, Olson K, Klassen P, Chertow GM. Effects of the calcimimetic cinacalcet HCl on cardiovascular disease, fracture, and health-related quality of life in secondary hyperparathyroidism. Kidney Int. 2005;68(4):1793–800.

    CAS  PubMed  Google Scholar 

  70. Investigators ET, Chertow GM, Block GA, Correa-Rotter R, Drueke TB, Floege J, et al. Effect of cinacalcet on cardiovascular disease in patients undergoing dialysis. N Engl J Med. 2012;367(26):2482–94.

    Google Scholar 

  71. Malluche HH, Monier-Faugere MC, Wang G, Fraza OJ, Charytan C, Coburn JW, et al. An assessment of cinacalcet HCl effects on bone histology in dialysis patients with secondary hyperparathyroidism. Clin Nephrol. 2008;69(4):269–78.

    CAS  PubMed  Google Scholar 

  72. Behets GJ, Spasovski G, Sterling LR, Goodman WG, Spiegel DM, De Broe ME, et al. Bone histomorphometry before and after long-term treatment with cinacalcet in dialysis patients with secondary hyperparathyroidism. Kidney Int. 2015;87(4):846–56.

    CAS  PubMed  Google Scholar 

  73. Barreto FC, Barreto DV, Moyses RM, Neves KR, Canziani ME, Draibe SA, et al. K/DOQI-recommended intact PTH levels do not prevent low-turnover bone disease in hemodialysis patients. Kidney Int. 2008;73(6):771–7.

    CAS  PubMed  Google Scholar 

  74. • Sprague SM, Bellorin-Font E, Jorgetti V, Carvalho AB, Malluche HH, Ferreira A, 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):559–66. This study, one of the largest bone biopsy studies evaluating serum bone biomarkers (PTH, bone alkaline phosphatase bALP, PINP) for the prediction of bone histomorphometry, shows that iPTH and bALP had the best discriminating ability (although suboptimal) to predict high or low bone turnover, and that iPTH continues to be the best available tool to discriminate bone turnover in CKD patients on dialysis. In addition, iPTH had relatively high specificity, although lower sensitivity, to detect low turnover and high turnover utilizing the KDIGO-recommended cutoff of less than 2 times the upper limit of normal and more than 9 times the upper limit of normal in differentiating high bone turnover.

    PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Kevin J. Martin.

Ethics declarations

Conflict of Interest

Ezequiel Bellorin-Font and George Vasquez- Rios declare no conflict of interest.

Kevin Martin reports personal fees from Amgen, outside the submitted work.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

This article is part of the Topical Collection on Kidney and Bone

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Bellorin-Font, E., Vasquez-Rios, G. & Martin, K.J. Controversies in the Management of Secondary Hyperparathyroidism in Chronic Kidney Disease. Curr Osteoporos Rep 17, 333–342 (2019). https://doi.org/10.1007/s11914-019-00533-x

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11914-019-00533-x

Keywords

Navigation