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The Role of Osteopontin in the Development of Albuminuria

Johan Lorenzen^*, Rajshree Shah^*, Alisha Biser^*, Serban A. Staicu^*, Thiruvur Niranjan^*, Ana Maria Garcia^*, Antje Gruenwald^*, David B. Thomas, Ibrahim F. Shatat, Katarine Supe, Robert P. Woroniecki and Katalin Susztak^*

Division of Nephrology, Departments of ^* Medicine, Pathology, and Pediatrics, Albert Einstein College of Medicine, Bronx, New York

Correspondence: Dr. Katalin Susztak, Division of Nephrology, Albert Einstein College of Medicine, Bronx, NY 10461. Phone: 718-430-3498; Fax: 718-430-8963; E-mail: ksusztak{at}aecom.yu.edu

Received for publication April 20, 2007. Accepted for publication February 22, 2008.

Several gene array studies have suggested that osteopontin (Opn) expression strongly correlates with albuminuria and glomerular disease. Urinary Opn concentration and kidney Opn immunoreactivity were found to be increased in patients with steroid-sensitive nephrotic syndrome. In addition, renal Opn mRNA was increased in the Ins2^Akita mouse model of type 1 diabetic nephropathy, in the LPS-induced albuminuria model, and in glomeruli of puromycin aminonucleotide–induced nephrotic rats. Opn knockout mice did not develop albuminuria in response to LPS injection, and Opn knockout mice were protected from diabetes-induced albuminuria and mesangial expansion. In the glomerulus, Opn immunostaining was increased specifically in podocytes. Treatment of podocytes with recombinant Opn activated the NF-B pathway, increased expression of urokinase plasminogen activator and matrix metalloproteinases 2 and 9, and increased podocyte motility. Taken together, these results indicate that Opn plays an important role in the development of albuminuria, possibly by modulating podocyte signaling and motility.

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673