Mouse models have been widely used to understand kidney disease pathomechanisms and play an important role in drug discovery. However, these models have not been systematically analyzed and compared.

Here, we characterized 18 different mouse kidney disease models at both bulk and single-cell gene expression levels. Our analysis revealed that cell fraction changes are major drivers of bulk gene expression differences. While single-cell level gene expression changes were mostly model-specific, different disease models showed similar changes when compared at a pathway level.

We also compared mice to patient samples. The mouse diabetic kidney disease model only showed a small number of conserved genes when compared to patients, but we observed pathway-level conservation between mouse and human diabetic samples.