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Can Hyperparathyroid Bone Disease Be Arrested or Reversed?

Nephrological Department P, Rigshospitalet and Nephrological Department B, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark

Address correspondence to: Dr. Klaus Olgaard, University of Copenhagen, Department of Nephrology, P2132, Rigshospitalet, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark. Phone: +45-3545-2130; Fax: +45-3545-2672; E-mail: olgaard{at}rh.dk

Parathyroid hyperplasia, oversecretion of parathyroid hormone (PTH), and hyperparathyroid bone disease are characteristic features of chronic uremia; they develop early in the course of uremia and often in a progressive way. This review focuses on the potential for arrest or regression of hyperparathyroid-induced bone disease. For this purpose, the review addresses investigations that have used bone histology and not investigations that indirectly attempted to demonstrate changes in the skeleton by measurements of bone mineral density or laboratory indices of bone turnover, other than PTH. A prerequisite for inducing regression of the hyperparathyroid bone disease is a significant suppression of PTH secretion or reversal of hyperparathyroidism and uremia. It is concluded, on the basis of paired bone biopsy studies in patients with established hyperparathyroid bone disease, that bone histology can be improved or normalized after treatment that diminishes PTH levels. Oversuppression of PTH levels, however, might lead to adynamic bone disease.

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				K. Olgaard and E. Lewin Use (or misuse) of vitamin D treatment in CKD and dialysis patients: A recent meta-analysis on vitamin D compounds in chronic kidney disease [1] and an editorial comment [2] accompanying this meta-analysis have already been published. We believe that these papers deserve some comments in the interest of the NDT readership Nephrol. Dial. Transplant., June 1, 2008; 23(6): 1786 - 1789. [Full Text] [PDF]