Journal of Bone and Mineral Metabolism

, Volume 24, Issue 6, pp 434–438

The kidney and bone metabolism: Nephrologists' point of view

Authors

    • Division of Nephrology and Dialysis CenterKobe University School of Medicine
  • Yasuhiro Hamada
    • Division of Nephrology and Dialysis CenterKobe University School of Medicine
  • Shohei Nakanishi
    • Division of Nephrology and Dialysis CenterKobe University School of Medicine
    • Division of NephrologyToranomon Branch Hospital
  • Motoko Tanaka
    • Department of NephrologyAkebono Clinic
REVIEW ARTICLE

DOI: 10.1007/s00774-006-0719-7

Cite this article as:
Fukagawa, M., Hamada, Y., Nakanishi, S. et al. J Bone Miner Metab (2006) 24: 434. doi:10.1007/s00774-006-0719-7

Abstract

The kidney plays an important role in the regulatory system for bone and mineral metabolism. In chronic kidney disease (CKD), various abnormalities, recently named CKD-mineral and bone disorder (CKD-MBD), may develop in this system. The optimal management of CKD-MBD should be achieved without increasing the risk of metastatic calcification, including that of blood vessels. Thus, it is quite important to identify severe cases of hyperparathyroidism refractory to medical therapy. The size of the parathyroid glands, serum levels of fibroblast growth factor (FGF)23, and, possibly, the overproduction of a novel form of parathyroid hormone (PTH), serve as useful markers for this purpose. Adynamic bone disease with low buffering capacity for calcium is another major cause of hypercalcemia in dialysis patients. Our recent studies suggest that indoxyl sulfate accumulated in uremic serum is responsible for the suppression of osteoblastic function. In order to maintain the bone quality in patients with CKD, bone changes due to aging, menopause, and malnutrition need to be considered by nephrolgists and non-nephrologists in collaboration.

Key words

kidney chronic kidney disease CKD-MBD parathyroid PTH FGF23 indoxyl sulfate

Copyright information

© Springer-Verlag Tokyo 2006