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NDT Advance Access originally published online on May 15, 2006
Nephrology Dialysis Transplantation 2006 21(8):2075-2077; doi:10.1093/ndt/gfl245
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Translational Nephrology

Anti-RANKL therapy—implications for the bone-vascular-axis in CKD? Denosumab in post-menopausal women with low bone mineral density*

Ralf Westenfeld, Markus Ketteler and Vincent M. Brandenburg

RWTH University Hostipal, Nephrology and Iumunology, Aachen, NRW, Germany

Correspondence and offprint requests to: Ralf Westenfeld, MD, Department of Nephrology and Clinical Immunology, University Hospital Aachen, Pauwelsstrasse 30, D-52057 Aachen, Germany. Email: ralf.westenfeld@rwth-aachen.de

Keywords: chronic kidney disease; osteoporosis; osteoprotegerin; RANKL; vascular calcification

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

Less than a decade ago substantial changes in our understanding of bone metabolism emerged by the discovery of the outstanding importance of the osteoprotegerin (OPG)–receptor activator of nuclear factor-{kappa}B (RANK)—RANK ligand (RANKL) system for bone cell regulatory processes. The OPG–RANK–RANKL axis is the biochemical correlate for the well-known ‘coupling’ in bone remodelling: a strongly linked interplay between continuously ongoing bone degradation and bone formation—in other words between osteoblastic and osteoclastic activity [1,2].

In this locally active, triangular system, RANKL exerts the action of an osteoclastic activator, enhancing both differentiation as well as functional status of osteoclasts and hence increasing bone resorptive activity. In contrast, osteoprotegerin (nomen est omen) functions as a soluble decoy receptor for RANKL and thus antagonizes RANKL action with the net effect of bone . . . [Full Text of this Article]


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