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NDT Plus Advance Access published online on September 30, 2009
NDT Plus, doi:10.1093/ndtplus/sfp138
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© The Author 2009. Published by Oxford University Press [on behalf of ERA-EDTA]. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Marked increase in bone formation markers after cinacalcet treatment by mechanisms distinct from hungry bone syndrome in a haemodialysis patient

Shunsuke Goto1, Hideki Fujii1, Yutaka Matsui2 and Masafumi Fukagawa1

1 Division of Nephrology and Kidney Center, Kobe University School of Medicine, Kobe
2 Matsui-clinic, Akashi, Japan

Correspondence: Masafumi Fukagawa; E-mail: fukagawa{at}med.kobe-u.ac.jp


  Abstract

A 59-year-old female who was on dialysis due to diabetic nephropathy was referred to our hospital for severe hyperparathyroidism refractory to intravenous vitamin D receptor activator treatment. With subsequent cinacalcet hydrochloride treatment, parathyroid hormone (PTH) levels were only slightly suppressed. However, progressive increases were observed in serum alkaline phosphatase (ALP) and bone-specific alkaline phosphatase (BAP) levels with mild hypocalcaemia. A bone biopsy, obtained immediately before surgical parathyroidectomy after 3 months of cinacalcet treatment, revealed no disappearance of osteoclasts. These data suggest that cinacalcet hydrochloride treatment may induce a marked promotion of bone formation by mechanisms distinct from hungry bone syndrome that usually develops after parathyroidectomy.

Key Words: bone formation • cinacalcet hydrochloride • secondary hyperparathyroidism

Received for publication June 2, 2009. Accepted for publication August 28, 2009.


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