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Role of Xanthine Oxidase in Passive Heymann Nephritis in Rats

WILFRIED GWINNER^*, JENS PLASGER^*, RALF P. BRANDES, BIRGIT KUBAT, MATTHIAS SCHULZE^*, HEINZ REGELE^§, DONTSCHO KERJASCHKI^§, CHRISTOPH J. OLBRICHT^* and KARL-MARTIN KOCH^*

^* Division of Nephrology, Department of Internal Medicine, Medical School Hannover, Hannover; Germany
Department of Anatomy, Medical School Hannover, Hannover; Germany
Institut für Kardiovaskuläre Physiologie, Klinik der Johann-Wolfgang-Goethe Universität, Frankfurt, Germany
^§ Division of Ultrastructural Pathology and Cell Biology, Institute of Clinical Pathology, University of Vienna, Vienna, Austria.

Correspondence to Dr. Wilfried Gwinner, Medical School of Hannover, Department of Internal Medicine, Carl-Neuberg-Strasse 1, D-30625 Hannover, Germany. Phone: 49 511 532 4446; Fax: 49 511 55 23 66; E-mail: WGwinner{at}t-online.de

Abstract. Passive Heymann nephritis (PHN) in rats is a model of human membranous nephropathy characterized by formation of subepithelial immune deposits in the glomerular capillary wall and complement activation. Oxygen radicals have been implicated in the subsequent glomerular damage which leads to proteinuria. This study examines the involvement of xanthine oxidase in this process. Xanthine oxidase activity was increased nearly twofold in glomeruli isolated 1 and 12 d after induction of PHN, and this was associated with increased glomerular superoxide anion generation. Analysis of glomerular samples by Northern and Western blotting revealed no quantitative changes in xanthine oxidoreductase expression in PHN, suggesting conversion of xanthine dehydrogenase to the oxidase form as the cause of increased activity. Treatment of rats with tungsten, an inhibitor of xanthine oxidase, before induction of PHN resulted in a marked decrease in glomerular xanthine oxidase activity and superoxide anion generation, and decreased proteinuria by 80% (day 12: 423 ± 245 mg/d in PHN versus 78 ± 53 mg/d in tungsten-treated PHN animals, P < 0.01). These findings point to a pivotal role of xanthine oxidase in the pathophysiology of PHN and could be of importance in the therapy of human membranous nephropathy.

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