To validate these findings in an alternative model of CKD, independent of potential confounding effects of adenine,44 we used a mouse model of human Alport disease (Col4a3−/− mice).32,45 Because disease progression in Col4a3−/− models is strain dependent, we selected slower-progressing C57BL6J/Col4a3−/− mice that are known to eventually develop LVH.45,46 By 20 weeks of age, Col4a3−/− mice exhibited LVH and changes in mitochondrial morphology (Supplementary Figure S2). The gene discussed is COL4A3; the disease is chronic kidney disease.