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Identification of a Unique Transgenic Mouse Line That Develops Megabladder, Obstructive Uropathy, and Renal Dysfunction

Sunita Singh^*, Melissa Robinson^*, Fatin Nahi^*, Brian Coley, Michael L. Robinson, Carlton M. Bates^*, Karl Kornacker and Kirk M. McHugh^*

^* Center for Cell and Developmental Biology, Columbus Children’s Research Institute and Department of Radiology, Columbus Children’s Hospital and Division of Sensory Biophysics, The Ohio State University, Columbus, and Zoology Department, Miami University, Oxford, Ohio

Address correspondence to: Dr. Kirk M. McHugh, Columbus Children’s Research Institute, 700 Children’s Drive, Suite WA 2014, Columbus, OH 43205. Phone: 614-355-2817; Fax: 614-722-5892; mchughk{at}ccri.net

Received for publication April 27, 2006. Accepted for publication November 7, 2006.

Urinary tract malformations, obstructive uropathy, and hypoplasia/dysplasia are extremely important in terms of pediatric health care costs, with end-stage renal failure in children estimated to cost >$15 billion annually in the United States alone. Even so, little is known regarding the mechanisms that control these processes. Identified was a unique mutant mouse model that develops in utero megabladder, resulting in variable hydroureteronephrosis and chronic renal failure secondary to obstructive uropathy. These animals, designated mgb for megabladder, possess a primary defect in bladder smooth muscle development that is apparent by embryonic day 15. The mgb mouse represents an excellent model for the study of normal and pathogenic bladder development, including the postnatal progression of chronic renal failure that results from the development of in utero obstructive uropathy.

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