ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2025
Sex-specific cardiac dysfunction in mice with chronic kidney disease.
Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Review
- Identification of end-stage renal disease-associated loci in X chromosome: an X chromosome-wide association study.MedScience · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
backgroundCardiovascular disease (CVD) is the leading cause of death among patients with chronic kidney disease (CKD). Rodent models are widely used to study uremic CVD pathophysiology. We compared cardiac function parameters in male and female animals from two established mouse CKD models and examined associations between gut-derived uremic toxins and echocardiogram findings.
methodsMale and female adult C57Bl/6J mice were randomly assigned to control, adenine-induced CKD and 5/6 nephrectomy CKD groups. Echocardiography was performed on all mice at age 17 weeks (5 weeks after CKD induction). Serum creatinine, cystatin C and gut-derived uremic toxins were analyzed at study termination, and RNA sequencing of left ventricle tissue was performed and analyzed.
resultsMarkers of kidney dysfunction were elevated in both CKD models. The gut-derived uremic toxin indoxyl sulfate was increased in both CKD models, while trimethylamine N-oxide was increased in adenine CKD mice and p-cresyl sulfate in nephrectomy animals. Left ventricular volume was increased in nephrectomy animals. Cardiac output was decreased in male CKD animals from both models compared with controls, and ejection fraction was decreased in male 5/6 nephrectomy mice. Female controls had lower stroke volume and cardiac output than male counterparts, and female CKD animals had preserved cardiac output and ejection fraction when compared with female controls. The gut-derived uremic toxins trimethylamine N-oxide and indoxyl sulfate correlated with decreased cardiac output in male animals. Transcriptomics of cardiac tissue revealed sex-based variations in matrix metalloproteinase and mitochondrial pathways associated with cardiac dysfunction.
conclusionsOur work highlights sex differences in cardiac function and serum chemistries in two established preclinical CKD models. Gut-derived uremic toxins may impact cardiorenal pathophysiology and low cardiac output in male CKD animals.
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