Skip Navigation

This Article
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 (9)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Fukagawa, M.
Right arrow Articles by Kurokawa, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fukagawa, M.
Right arrow Articles by Kurokawa, K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrol Dial Transplant (2002) 17: 2-5
© 2002 European Renal Association-European Dialysis and Transplant Association


Renal osteodystrophy and secondary hyperparathyroidism

Masafumi Fukagawa1,, Junichiro J. Kazama2 and Kiyoshi Kurokawa3

1 Division of Nephrology and Dialysis Center, Kobe University School of Medicine, Kobe, Japan, 2 Division of Nephrology, Niigata University School of Medicine, Niigata, Japan and 3 Tokai University School of Medicine, Isehara, Japan

Abstract

Secondary hyperparathyroidism with marked parathyroid hyperplasia is the major type of renal osteodystrophy. In addition to classic stimuli for parathyroid hormone (PTH) such as decreased concentrations of ionized calcium and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3, calcitriol), several mechanisms have been suggested. Those include decreased density of calcitriol and calcium-sensing receptors, as well as the direct action of phosphate. Skeletal resistance to PTH was initially recognized as a blunted calcaemic action of PTH, which has been considered another stimulus for PTH secretion. Once suppression of PTH became possible by newly developed therapeutic modalities, it has been shown that this background abnormality plays an important role in the development of adynamic bone disease in uraemic patients. However, the mechanism of skeletal resistance to PTH has not been fully elucidated yet, but recent papers suggested that osteoprotegerin (OPG) accumulating in uraemic serum might inhibit osteoclastogenesis induced by PTH.

Keywords: chronic renal failure; osteoprotegerin; PTH; RANKL; renal osteodystrophy; vitamin D

Notes

Correspondence and offprint requests to: Masafumi Fukagawa, MD, PhD, FJSIM, Associate Professor and Director, Division of Nephrology and Dialysis Center, Kobe University School of Medicine, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan. Email: fukagawa{at}med.kobe\|[hyphen]\|u.ac.jp


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




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.