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NDT Advance Access published online on July 21, 2006
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfl330
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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
Received March 8, 2006
Accepted May 9, 2006

Brief Report

Does Tamm-Horsfall protein-uric acid binding play a significant role in urate homeostasis?

Michael S. Gersch 1 *, Yuri Y. Sautin 1, Christine M. Gersch 1, George Henderson 1, Lise Bankir 2, and Richard J. Johnson 1

1 University of Florida, Department of Medicine, Gainesville, Florida, USA
2 Institut National de la Sante et de la Recherche Médicale, Unit 652, Paris, France

* To whom correspondence should be addressed.
Michael S. Gersch, E-mail: gerscms{at}medicine.ufl.edu



  Abstract

Background. Mutations in Tamm-Horsfall protein (THP), also known as uromodulin, lead to a group of diseases known as the uromodulin storage disorders. Clinically, these diseases present with tubulo-interstitial damage, progressive renal dysfunction, hyperuricaemia, and gout. However, it remains unclear how a mutation in THP, a protein produced in the thick ascending limb, can cause hyperuricaemia when most of the uric acid transport is believed to occur in the proximal tubule. However, one study in humans suggests that uric acid could also be secreted in the distal tubule. Thus, an attractive hypothesis could be that THP would bind to uric acid in the distal tubule, and decrease its subsequent reabsorption in the distal nephron.

Methods. We screened for uric acid binding to THP using four independent binding assays.

Results. There was no evidence that uric acid could bind to THP.

Conclusion. THP-uric acid binding does not seem to play a significant role in the regulation of urate homeostasis.

Keywords: binding; familial juvenile hyperuricaemic nephropathy (FJHN); medullary cystic kidney disease (MCKD); thick ascending limb; uromodulin.
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