Abstract
Progress in the identification of causal genes and understanding of the mechanism underlying kidney disease is hindered by the almost exclusive use of a few animal models with restrictive monogenic backgrounds that may be more resistant to kidney disease compared with humans and, therefore, poor models. Exploring the large genetic diversity in classical animal models, such as mice and rats, and leveraging species diversity will allow us to use the genetic advantages of zebrafish, Drosophila, and other species, to develop both new animal models that are more relevant to the study of human kidney disease and potential therapies.
