ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: SA-PO962

Pathophysiology and Molecular Characterization of a Novel Model of CKD and Left Ventricular Diastolic Dysfunction (CKD-LVDD Model)

Session Information

  • CKD: Pathobiology - II
    November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2203 CKD (Non-Dialysis): Mechanisms


  • Chade, Alejandro R., The University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Eirin, Alfonso, Mayo Clinic Minnesota, Rochester, Minnesota, United States

Chronic kidney disease (CKD) is an independent risk factor for the development of heart failure, but the underlying mechanisms remain unknown. We developed a translational swine model of CKD and left ventricular diastolic dysfunction (CKD-LVDD) that replicates human disease and showed that cardiac abnormalities associate with a marked renal release of inflammatory cytokines to the systemic circulation, suggesting a potential pathophysiological connection. We examined whether the cardiac transcriptomic landscape is altered in CKD-LVDD pigs compared to normal controls.


CKD-LVDD and normal pigs (n=6 each) were studied for 14 weeks. Cardiac morphology and function (echocardiography) and renal hemodynamics (multi-detector CT) were quantified in vivo. mRNA-sequencing studies were performed (n=3 each) and expression profiles for dysregulated (fold change >1.4 or <0.7 and p<0.05) mRNAs in CKD-LVDD pigs were functionally interpreted by gene ontology analysis. Cardiac remodeling, inflammation, calcium cycling, and mitochondrial morphology.


Cardiac abnormalities in CKD-LVDD were associated to differentially expressed calcium signaling, mitochondrial, and inflammatory genes, accompanied by cardiac fibrosis, mitochondrial damage, M1 macrophage infiltration, and altered calcium cycling vs. normal controls.


Our integrated pathophysiology and molecular data from a translational model of disease may set the stage for future specific interventions to ameliorate the development of LVDD in CKD.


  • NIDDK Support