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Am J Physiol Renal Physiol 296: F213-F229, 2009. First published September 10, 2008; doi:10.1152/ajprenal.90421.2008
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REVIEW

Inducible rodent models of acquired podocyte diseases

Jeffrey W. Pippin,1 Paul T. Brinkkoetter,1 Fionnualla C. Cormack-Aboud,1 Raghu V. Durvasula,1 Peter V. Hauser,1 Jolanta Kowalewska,2 Ronald D. Krofft,1 Christine M. Logar,1 Caroline B. Marshall,1 Takamoto Ohse,1 and Stuart J. Shankland1

1Division of Nephrology, Department of Medicine, and 2Department of Pathology, University of Washington School of Medicine, Seattle, Washington

Submitted 17 July 2008 ; accepted in final form 8 September 2008

ABSTRACT

Glomerular diseases remain the leading cause of chronic and end-stage kidney disease. Significant advances in our understanding of human glomerular diseases have been enabled by the development and better characterization of animal models. Diseases of the glomerular epithelial cells (podocytes) account for the majority of proteinuric diseases. Rodents have been extensively used experimentally to better define mechanisms of disease induction and progression, as well as to identify potential targets and therapies. The development of podocyte-specific genetically modified mice has energized the research field to better understand which animal models are appropriate to study acquired podocyte diseases. In this review we discuss inducible experimental models of acquired nondiabetic podocyte diseases in rodents, namely, passive Heymann nephritis, puromycin aminonucleoside nephrosis, adriamycin nephrosis, liopolysaccharide, crescentic glomerulonephritis, and protein overload nephropathy models. Details are given on the model backgrounds, how to induce each model, the interpretations of the data, and the benefits and shortcomings of each. Genetic rodent models of podocyte injury are excluded.

glomerulus; animal models


Address for reprint requests and other correspondence: J. W. Pippin, Univ. of Washington School of Medicine, 1959 NE Pacific St., Box 356521, Seattle, WA 98195 (e-mail: scoobie{at}u.washington.edu)




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