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NDT Advance Access originally published online on April 20, 2007
Nephrology Dialysis Transplantation 2007 22(7):1828-1839; doi:10.1093/ndt/gfm177
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© The Author 2007
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Can calcimimetics inhibit parathyroid hyperplasia? Evidence from preclinical studies

Tilman Drueke1, David Martin2 and Mariano Rodriguez3

1Inserm Unit 845 and Division of Nephrology, Necker Hospital, University Paris 5, Paris, France, 2Amgen Inc., Department of Metabolic Disorders, Thousand Oaks, CA, USA and 3Research Unit, Nephrology Service, Hospital Universitario Reina Sofia, Cordoba, Spain

Correspondence and offprint requests to: Dr D. Martin, PhD, Department of Metabolic Disorders, Amgen Inc., One Amgen Center Drive, Thousand Oaks, CA 91320-1799, USA. Email: dmartin@amgen.com

Keywords: calcimimetics; calcium receptor; chronic renal insufficiency; hyperparathyroidism; parathyroid hyperplasia

The first 150 words of the full text of this article appear below.



   Introduction
 
The cells of the parathyroid gland secrete parathyroid hormone (PTH), which plays a pivotal role in maintaining circulating levels of ionized calcium (Ca2+) within a narrow physiological range. The main actions of PTH include (i) releasing calcium and phosphorus from bone, (ii) decreasing renal calcium excretion, (iii) increasing urinary phosphorus excretion and (iv) stimulating renal production of calcitriol (1,25- dihydroxy vitamin D3), the active form of vitamin D. Vitamin D and its receptors (VDRs) also play key roles in calcium homeostasis: vitamin D acts on VDRs in the intestine to increase calcium absorption, and on VDRs in parathyroid cells to inhibit PTH mRNA synthesis [1].

Secondary hyperparathyroidism (SHPT) represents an adaptive response to the progressively impaired control of calcium, phosphorus and vitamin D in chronic kidney disease (CKD). It is characterized by parathyroid hyperplasia and excessive synthesis and secretion of PTH, resulting in excessive bone resorption, soft-tissue . . . [Full Text of this Article]



   Pathophysiological aspects of parathyroid hyperplasia
 
The role of the calcium-sensing receptor in SHPT
Calcimimetics in SHPT
Effects on parathyroid hyperplasia
Effects on CaR and VDR expression


   Effects of other SHPT treatments on parathyroid hyperplasia
 


   Conclusions
 

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