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Published on: December 20, 2014
Vesicoureteric reflux and reflux nephropathy: from mouse models to childhood disease
Marie-Lyne Fillion1, Christine L Watt, Indra R Gupta
1Department of Human Genetics, McGill University, Montreal, Quebec, Canada.
Insights
Vesicoureteric reflux (VUR) in children can lead to kidney infections and scarring. Mouse models of VUR and reflux nephropathy offer insights into disease development and potential human genetic factors.
Area of Science:
- Pediatric Nephrology
- Urology
- Genetics
Background:
- Vesicoureteric reflux (VUR) is a common congenital defect in children.
- VUR predisposes individuals to recurrent kidney infections, potentially causing renal scarring or reflux nephropathy.
- Reflux nephropathy, characterized by inflammation and fibrosis, is a significant cause of end-stage renal failure.
Purpose of the Study:
- To explore the pathogenesis of VUR and reflux nephropathy.
- To identify genes and phenotypes relevant to human studies using animal models.
- To advance understanding of congenital urinary tract defects.
Main Methods:
- Utilizing established mouse models that exhibit VUR.
- Employing models that develop reflux nephropathy.
- Comparative analysis of genetic and phenotypic data.
Main Results:
- Mouse models successfully replicate key features of VUR and reflux nephropathy.
- These models facilitate the study of disease mechanisms.
- Potential genetic and phenotypic targets for human research have been identified.
Conclusions:
- Mouse models are valuable tools for investigating VUR and reflux nephropathy.
- Further research in these models can elucidate disease pathways.
- Insights gained may inform human genetic studies and clinical management.
Abstract:
Vesicoureteric reflux (VUR) is a common congenital urinary tract defect that predisposes children to recurrent kidney infections. Kidney infections can result in renal scarring or reflux nephropathy defined by the presence of chronic tubulo-interstitial inflammation and fibrosis that is a frequent cause of end-stage renal failure. The discovery of mouse models with VUR and with reflux nephropathy has provided new opportunities to understand the pathogenesis of these conditions and may provide insight on the genes and the associated phenotypes that need to be examined in human studies.
