Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (7)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Schroeder, N. J.
Right arrow Articles by Cunningham, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schroeder, N. J.
Right arrow Articles by Cunningham, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrol Dial Transplant (2000) 15: 460-466
© 2000 European Renal Association-European Dialysis and Transplant Association

Invited Comments

What's new in vitamin D for the nephrologist?

Neil J. Schroeder and John Cunningham

Department of Renal Medicine and Transplantation, Royal London Hospital, Whitechapel, London, UK

Correspondence and offprint requests to: Dr J. Cunningham, Department of Renal Medicine and Transplantation, Royal London Hospital, Whitechapel, London E1 1BB, UK.

Introduction

In this review we discuss some of the clinical implications of progress in our understanding of the action of vitamin D and its derivatives on calcium, phosphate homeostasis and skeletal function in uraemia.

The parathyroid glands synthesize and secrete parathyroid hormone (PTH) in response to low calcium, low 1,25-dihydroxyvitamin D3 (calcitriol), and high phosphate concentrations. The interplay between these elements is complex, operating through several feedback mechanisms. Both PTH and calcitriol regulate circulating calcium and phosphate concentrations through their action on target organs, namely the kidney, bone, and intestine. PTH and calcitriol regulate one another's production, and additionally are both regulated separately by extracellular calcium and phosphate, as schematically illustrated in Figure 1Go. The impairment of phosphate excretion and of calcitriol synthesis that accompanies renal insufficiency results in increased parathyroid stimulation from each of the principal modulators, namely decreased calcium, increased phosphate, and decreased calcitriol. This scenario is further . . . [Full Text of this Article]

The vitamin D receptor

Calcitriol and the parathyroids

PTH synthesis and secretion
Parathyroid cell proliferation
Calcitriol and the kidney

Calcitriol and the intestine

Calcitriol, calcitriol derivatives and bone

Clinical developments

Current therapies
New analogues
22-oxacalcitriol (OCT)
1-alpha-hydroxy vitamin D2
Paricalcitol
Falecalcitriol
Summary

Acknowledgments

References


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Nephrol Dial TransplantHome page
F. Locatelli, J. B. Cannata-Andia, T. B. Drueke, W. H. Horl, D. Fouque, O. Heimburger, and E. Ritz
Management of disturbances of calcium and phosphate metabolism in chronic renal insufficiency, with emphasis on the control of hyperphosphataemia
Nephrol. Dial. Transplant., May 1, 2002; 17(5): 723 - 731.
[Abstract] [Full Text] [PDF]