Serum calcium and bone: effect of PTH, phosphate, vitamin D and uremia.

Abstract

Hyperparathyroidism develops in chronic kidney disease (CKD). A decreased calcemic response to parathyroid hormone (PTH) contributes to the development of hyperparathyroidism and is presumed due to reduced calcium efflux from bone. Contributing factors to the decreased calcemic response to PTH in CKD include: 1) hyperphosphatemia; 2) decreased serum calcitriol; 3) downregulation of the PTH1 receptor; 4) large, truncated amino-terminal PTH fragments acting at the carboxy-PTH receptor; and 5) uremic toxins. Also, prolonged high dose calcitriol administration may decrease the exchangeable pool of bone calcium independent of PTH. The goal of the review is to provide a better understanding of how the above cited factors affect calcium efflux from bone in CKD. In conclusion, much remains to be learned about the role of bone in the regulation of serum calcium.

• Authors: Barton S Levine, Mariano Rodríguez, Arnold J Felsenfeld
• Journal: Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia (Nefrologia) Vol. 34 Issue 5 Pg. 658-69 ( 2014) ISSN: 1989-2284 [Electronic] Spain
• PMID: 25259820 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Parathyroid Hormone
• Phosphates
• Vitamin D
• Calcium

Topics

• Bone and Bones (metabolism)
• Calcium (blood, metabolism)
• Humans
• Parathyroid Hormone (pharmacology, physiology)
• Phosphates (pharmacology, physiology)
• Uremia (metabolism)
• Vitamin D (pharmacology, physiology)