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NDT Advance Access published online on May 9, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn260
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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


The bone-renal axis in early chronic kidney disease: an emerging paradigm

John Danziger1

Renal Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA

Correspondence and offprint requests to: John Danziger, 330 Brookline Ave E/DA517, Boston, MA 02215, USA. Tel: +1-617-667-2147; Fax: +1-617-667-5276; E-mail: jdanzige@bidmc.harvard.edu

Keywords: chronic kidney disease; FGF-23; parathyroid; phosphaturia; phosphorus

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



   Introduction
 
The prevailing paradigm of mineral metabolism in chronic kidney disease (CKD) is based on two principles. First, as the tradeoff hypothesis suggests, phosphate retention leads to hyperparathyroidism, a response that maintains normal levels of serum phosphorus until relatively late in the CKD process [1–3]. In addition, it is believed that dietary deficiency of 25 hydroxylated vitamin D (25OHD) is important in early CKD, with the deficiency of the activated version, 1,25-hydroxylated vitamin D (1,25OHD), developing only in the later stages. Since the hydroxylation to 1,25OHD is considered to be a renal-dependent mechanism, the deficiency of this activated form is thought to reflect renal dysfunction. Various mechanisms have been impugned, including loss of renal mass, hyperparathyroidism, hyperphosphatemia and uremic toxins. These two principles have shaped the current KDOQI guidelines for the treatment of mineral metabolism in CKD.

However, more recent data suggest that this approach to mineral metabolism in . . . [Full Text of this Article]

FGF-23
The importance of FGF-23 in normal physiology
FGF-23 in early CKD
Effect of increasing FGF-23 on 1,25OHD levels
Systemic effects of FGF-23 elevation and 1,25OHD deficiency


   Conclusion
 

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