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J Am Soc Nephrol 14:139-147, 2003
© 2003 American Society of Nephrology

Osteopontin Is a Critical Inhibitor of Calcium Oxalate Crystal Formation and Retention in Renal Tubules

Jeffrey A. Wesson*, Richard J. Johnson§, Marrilda Mazzali{dagger}, Anne M. Beshensky*, Susan Stietz{dagger}, Ceci Giachelli{dagger}, Lucy Liaw{dagger}, Charles E. Alpers{dagger}, William G. Couser{dagger}, Jack G. Kleinman* and Jeremy Hughes{dagger}

*Department of Veterans Affairs Medical Center and Medical College of Wisconsin, Milwaukee, Wisconsin; {dagger}University of Washington, Seattle, Washington; {ddagger}Maine Medical Center Research Institute, University of Maine, Maine; §Baylor College of Medicine, Houston, Texas.

Correspondence to Dr. Jeremy Hughes, Phagocyte Laboratory, MRC Center for Inflammation Research, University of Edinburgh Medical School, Teviot Place, Edinburgh, EH8 9AG, United Kingdom. Phone: 44-131-6511574; Fax: 44-131-6511607;

ABSTRACT. Calcium nephrolithiasis is the most common form of renal stone disease, with calcium oxalate (CaOx) being the predominant constituent of renal stones. Current in vitro evidence implicates osteopontin (OPN) as one of several macromolecular inhibitors of urinary crystallization with potentially important actions at several stages of CaOx crystal formation and retention. To determine the importance of OPN in vivo, hyperoxaluria was induced in mice targeted for the deletion of the OPN gene together with wild-type control mice. Both groups were given 1% ethylene glycol, an oxalate precursor, in their drinking water for up to 4 wk. At 4 wk, OPN-deficient mice demonstrated significant intratubular deposits of CaOx crystals, whereas wild-type mice were completely unaffected. Retained crystals in tissue sections were positively identified as CaOx monohydrate by both polarized optical microscopy and x-ray powder diffraction analysis. Furthermore, hyperoxaluria in the OPN wild-type mice was associated with a significant 2- to 4-fold upregulation of renal OPN expression by immunocytochemistry, lending further support to a renoprotective role for OPN. These data indicate that OPN plays a critical renoprotective role in vivo as an inhibitor of CaOx crystal formation and retention in renal tubules. E-mail: jeremy.hughes@ed.ac.uk




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