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NDT Advance Access originally published online on July 6, 2004
Nephrology Dialysis Transplantation 2004 19(9):2228-2236; doi:10.1093/ndt/gfh302
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Nephrol Dial Transplant Vol. 19 No. 9 © ERA-EDTA 2004; all rights reserved

Original Article

Prevention of glomerular crescent formation in glomerulonephritis by mycophenolate mofetil in rats

Shin-ichi Takeda1,2, Masafumi Takahashi1, Yoshikazu Sado3, Koichi Takeuchi4, Yoji Hakamata1, Hisashi Shimizu1, Takashi Kaneko1, Hisashi Yamamoto2, Chiharu Ito2, Shigeo Ookawara4, Yasushi Asano2, Eiji Kusano2 and Eiji Kobayashi1

1 Division of Organ Replacement Research, Center for Molecular Medicine, 2 Division of Nephrology, Department of Medicine, 4 Department of Anatomy, Jichi Medical School, Tochigi and 3 Division of Immunology, Shigei Medical Research Institute, Okayama, Japan

Correspondence and offprint requests to: Masafumi Takahashi, MD, PhD, Division of Organ Replacement Research, Center for Molecular Medicine, Jichi Medical School, Minamikawachi-machi, Tochigi 329-0498, Japan. Email: masafumi{at}jichi.ac.jp

Background. Glomerular crescent formation is a prominent feature of aggressive forms of glomerulonephritis (GN) and is associated with a poor prognosis. We investigated whether the potent immunosuppressive agent mycophenolate mofetil (MMF) could prevent crescent formation in a model of anti-glomerular basement membrane (GBM) GN in the rat.

Methods. GN with glomerular crescents was induced by the injection of anti-GBM antibody to female Wistar–Kyoto (WKY/NCrj) rats. The experimental rats were divided into two groups: rats received vehicle (0.5% carboxymethylcerlose) or MMF (20 mg/kg/day) orally. Body weight was measured and the urine and blood samples were evaluated. The rats were sacrificed at day 14, and histological analysis was performed. The mRNA expression of cytokines and adhesion molecules in the kidney was analysed by reverse transcription–polymerase chain reaction (RT–PCR).

Results. Marked proteinuria, glomerular crescent formation and glomerulosclerosis were observed in this model, and these were significantly reduced by MMF treatment. Marked glomerular macrophage and T-cell infiltration was also observed, and MMF treatment significantly inhibited macrophage but not T-cell infiltration. RT–PCR and immunohistochemical analysis revealed that mRNA and protein expression of osteopontin was decreased by the treatment with MMF. In addition, MMF treatment in the early stages of GN could inhibit proteinuria, glomerular crescent formation and glomerulosclerosis.

Conclusions. These findings suggest therapeutic potential for MMF in the inhibition of glomerular crescent formation in GN and provide new insights into the mechanism underlying the amelioration of crescentic GN by MMF treatment.

Keywords: glomerular crescent formation; glomerulonephritis; immunosuppressant; inflammatory cells; osteopontin


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