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NDT Advance Access originally published online on August 9, 2005
Nephrology Dialysis Transplantation 2005 20(11):2358-2367; doi:10.1093/ndt/gfi062
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Original Article

Monoclonal antibody 1-22-3-induced glomerulonephritis in uninephrectomized rats as a model of progressive renal failure

Masayuki Tomita1, Hajime Sogabe1, Shoko Nakazato1, Shunji Nakatsuji2, Takahisa Noto1, Kaori Hamada1, Hiroshi Kawachi3, Fujio Shimizu3, Masahiko Matsuo1 and Seitaro Mutoh1

1 Medicinal Biology Research Laboratories, Fujisawa Pharmaceutical Co., Ltd, Osaka, Japan, 2 Toxicology Research Laboratories, Fujisawa Pharmaceutical Co., Ltd, 3 Department of Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan

Correspondence and offprint requests to: Masayuki Tomita, Pharmacology Research Laboratories, Astellas Pharma Inc., 1-6, Kashima 2-chome, Yodogawa-ku, Osaka 532-8514, Japan. Email: masayuki.tomita{at}jp.astellas.com

Background. At present, there are few available animal models of progressive renal failure originating from mesangial proliferative glomerulonephritis (GN). In the current study, we examined the usefulness of anti-Thy-1 monoclonal antibody (mAb) 1-22-3-induced GN in uninephrectomized rats as a model of progressive renal failure by analysing the similarities to human disease.

Methods. GN was induced by intravenous injection of mAb 1-22-3 into uninephrectomized male Wistar rats. The natural course of the disease was analysed in this model for 47 weeks. The effect of treatment with the angiotensin-converting enzyme inhibitor, captopril, on renal functional outcome was also examined in this model for 23 weeks, beginning from 1 week after antibody injection.

Results. Injection of mAb 1-22-3 induced a persistent proteinuria during the entire study period. Animals showed a progressive decline in renal function and 63% died by week 47. Severe glomerular and tubulointerstitial lesions were consistently observed. Treatment with captopril significantly inhibited increases in proteinuria and blood pressure, and attenuated renal injury. Captopril also retarded the progression of renal failure, and decreased mortality. Finally, the level of proteinuria was significantly correlated with the rate of decline in renal function, and the reduction in proteinuria by captopril was accompanied by a slower progression of renal failure.

Conclusions. The mAb 1-22-3-induced GN in a uninephrectomized rat model simulates the clinical manifestations of human disease, indicating that this model may be useful for studying progressive renal failure and for investigating new therapeutic strategies against renal failure.

Keywords: angiotensin-converting enzyme inhibitor; anti-Thy-1 antibody; captopril; mesangial proliferative glomerulonephritis; predictors of renal outcome; proteinuria


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