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NDT Advance Access originally published online on October 2, 2008
Nephrology Dialysis Transplantation 2009 24(1):28-30; doi:10.1093/ndt/gfn551
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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


Potential role of bone morphogenetic protein (BMP) signalling as a potential therapeutic target for modification of iron balance*

Sarah A. Browne and Donal Reddan

Division of Nephrology, Dept of Medicine, National University of Ireland (NUI), Galway, Ireland

Donal Reddan, Unit 1, Merlin Park University Hospital, Galway, Ireland. Tel: +35-3-91-775510; Fax: +35-3-91-720151; E-mail: donal.reddan@westernnephrology.com

Keywords: anaemia of chronic disease; bone morphogenetic proteins; hepcidin; iron metabolism; soluble haemojuvelin

The first 10% of the full text of this article appears below.



   Key findings in article to be discussed
 
This important paper by Babitt et al. outlines a novel method of regulating hepcidin expression that could potentially lead to novel methods of improving iron utilization amongst patients with anaemia of chronic kidney disease (CKD).

Hepcidin is the master regulator of systemic iron homeostasis acting by causing the internalization and degradation of the iron exporter channel, ferroportin. This blocks the efficient transfer of iron to plasma and therefore functionally blocks iron absorption [1,2,3]. Hepcidin also blocks the transfer of iron from the reticuloendothelial system to plasma in chronic inflammatory disease states [4]. Increased levels of hepcidin thus contribute to anaemia of inflammation by shunting iron away from erythropoiesis and sequestrating it in organs such as the liver and spleen [5]. Hepcidin deficiency itself can lead to haemochromatosis [6]. Babitt et al. . . . [Full Text of this Article]



   Review of field
 
What is in it for the practicing nephrologist?


   Take home message
 

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