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NDT Plus Advance Access originally published online on February 14, 2008
NDT Plus 2008 1(2):97-99; doi:10.1093/ndtplus/sfn008
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Calciphylaxis associated with chronic kidney disease and low bone turnover: management with recombinant human PTH-(1–34)

Grahame Elder and Karthic S. Kumar

Department of Renal Medicine, Westmead Hospital, Australia

Correspondence: Grahame Elder, Westmead Hospital-Department of Renal Medicine Westmead New South Wales 2145 Australia Tel: 61 2 98456962 Fax: 61 2 98685510, E-mail: g.elder@garvan.unsw.edu.au

Key Words: calciphylaxis • chronic kidney disease • low bone turnover • recombinant human PTH-(1–34) • bone turnover markers

Received for publication January 3, 2008. Accepted for publication January 14, 2008.

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   Introduction
 
In 1898 Bryant and White reported features of the condition that was later described as calciphylaxis by Selye in 1961 because of a pathophysiologic resemblance to anaphylaxis [1,2]. Calciphylaxis (or calcific uraemic arteriolopathy) is characterized by medial calcification of small arterioles, intimal proliferation, fibrosis and thrombosis resulting in ischaemia, necrosis and superinfection of the skin and subcutis. When renal function is normal, calciphylaxis has been reported infrequently, associated with conditions such as primary hyperparathyroidism [3]. However, amongst patients with chronic kidney disease (CKD) on dialysis, the annual incidence has been estimated at 1–4%, with an apparent increase over the past decades that may reflect the increased use of calcium-based phosphate binders [4,5]. For patients on dialysis, mortality rates are increased 8-fold if calciphylaxis develops [6]. The mortality of non-ulcerating types is ~. . . [Full Text of this Article]


   Case
 

   Discussion
 

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