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NDT Plus Advance Access originally published online on May 13, 2008
NDT Plus 2008 1(4):244-249; doi:10.1093/ndtplus/sfn036
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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

Hyperbaric oxygen as effective adjuvant therapy in the treatmentof distal calcific uraemic arteriolopathy

Natasha M. Rogers1,2, Sean H. Chang3, David J. O. Teubner4 and Patrick T. H. Coates1,2

1 Department of Nephrology and Transplantation Services, The Queen Elizabeth Hospital, University of Adelaide, Adelaide, South Australia 5011
2 Department of Medicine, University of Adelaide, North Terrace, Adelaide, South Australia 5000
3 ANZDATA Registry, The Queen Elizabeth Hospital, University of Adelaide, Adelaide, South Australia 5011
4 Hyperbaric Unit, The Royal Adelaide Hospital, Adelaide, South Australia 5000, Australia

Correspondence: P. T. H. Coates, Department of Nephrology and Transplantation Services, The Queen Elizabeth Hospital, 28 Woodville Road, Woodville, South Australia 5011, Australia. Tel: +61-8-8222-6000; Fax: +61-8-8222-8711; E-mail: toby.coates@nwahs.sa.gov.au

Key Words: calcific uraemic arteriolopathy • hyperbaric oxygen • renal failure

Received for publication March 11, 2008. Accepted for publication March 14, 2008.

The first 150 words of the full text of this article appear below.


   Introduction
 
Calcific uraemic arteriolopathy (CUA), calciphylaxis or uraemia of small-vessel disease is a rare life-threatening complication predominantly affecting patients with end-stage renal disease (ESRD) [1]. It typically occurs in those with secondary hyperparathyroidism and is associated with deranged calcium and phosphate metabolism. Other factors, such as malnutrition, obesity, diabetes mellitus, warfarin therapy and female gender, have been implicated as additional risk factors [2]. CUA presents as severely painful ulcers, usually occurring in the lower limbs. The mechanism of injury appears to be calcification of subcutaneous tissues and small arterioles. At a molecular level, derangement of vascular smooth muscle cell function leading to osteogenic differentiation in conjunction with endothelial cell dysfunction appears to be important [3]. The lesions are slow to heal, with superimposed bacterial infection leading to sepsis, the most common cause of death (in up to 80% of patients).

The first case series of . . . [Full Text of this Article]


   Methods
 

   Results
 

   Discussion
 

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