Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (25)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Malluche, H. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Malluche, H. H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrol Dial Transplant (2002) 17: 21-24
© 2002 European Renal Association-European Dialysis and Transplant Association


Aluminium and bone disease in chronic renal failure

Hartmut H. Malluche

University of Kentucky, Division of Nephrology, Bone and Mineral Metabolism, Lexington, KY 40536-1052, USA

Abstract

Aluminium is absorbed by the intestines and is rapidly transported into bone, where it disrupts mineralization and bone cell growth and activity. Its toxicities result in or exacerbate painful forms of renal osteodystrophy, most notably adynamic bone disease and osteomalacia, but also other forms of the disease. Because aluminium is sequestered in bone for long periods, its toxic effects are cumulative. As a result, even intermittent or low-dose use of aluminium-based phosphate binders adds to the total load of this toxin in the bone; thus, aluminium use is inadvisable, even for a ‘rescue indication’. Aluminium blood levels are not a reliable marker of aluminium absorption or organ load in dialysis patients: only stainable aluminium at the mineralization front reflects the histopathological changes observed in bone. Therefore, bone biopsies remain the only approach for definitive diagnosis of aluminium-related bone disease. Most importantly, lack of correlation between overall organ concentrations of a toxin, such as aluminium, and pathological changes does not rule out toxicity. Thus, the specific localization of the toxin is more important than overall organ concentration. What has been observed with aluminium during 25 years of research might be reproduced with other metals that are absorbed, transported and accumulated in bone. What we have learned about the toxicity of aluminium should inform our interpretation of data from studies of other metal-based therapeutics for renal patients. This calls for careful evaluation of any newly introduced therapeutic agents for bone disease in patients lacking excretory kidney function.

Keywords: accumulation; aluminium; bone; mineralization; osteodystrophy; osteomalacia

Notes

Correspondence and offprint requests to: Hartmut H. Malluche, MD, University of Kentucky, Division of Nephrology, Bone and Mineral Metabolism, 800 Rose St., Room MN 572, Lexington, KY 40536-1052, USA. Email: hhmall{at}uky.edu


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 NDT PlusHome page
A. L. M. de Francisco and F. Carrera
A New Paradigm for the Treatment of Secondary Hyperparathyroidism
NDT Plus, January 1, 2008; 1(suppl_1): i24 - i28.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.