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

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: TH-OR44

Renal Revascularization Attenuates Myocardial Mitochondrial Damage and Improves Diastolic Function in Pigs with Metabolic Syndrome and Renovascular Hypertension

Session Information

Category: Hypertension and CVD

  • 1403 Hypertension and CVD: Mechanisms

Authors

  • Eirin, Alfonso, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Farahani, Rahele A, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Ferguson, Christopher M., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Zhu, Xiang yang, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Tang, Hui, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Jordan, Kyra L., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Saadiq, Ishran M., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Herrmann, Sandra, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Chade, Alejandro R., The University of Mississippi Medical Center, Jackson, Mississippi, United States
  • Lerman, Amir, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Lerman, Lilach O., Mayo Clinic Minnesota, Rochester, Minnesota, United States
Background

Percutaneous transluminal renal angioplasty (PTRA) may improve renal and cardiac function in renovascular hypertension (RVH), but its effect on the biological mechanisms implicated in cardiac damage remains unknown. We hypothesized that restoration of kidney function by PTRA ameliorates myocardial mitochondrial damage and preserves cardiac function in pigs with metabolic syndrome (MetS) and RVH.

Methods

Pigs were studied after 16 weeks of MetS+RVH, MetS+RVH treated 4 weeks earlier with PTRA, and Lean and MetS Sham controls (n=6 each). Cardiac and renal function was assessed by multi-detector CT, whereas cardiac mitochondrial morphology and function, and injury pathways were assessed ex vivo.

Results

RVH induced renal and cardiac diastolic (albeit not systolic) dysfunction (Table). PTRA improved renal function but not RVH. It preserved myocardial mitochondrial structure and function, ameliorated oxidative stress and fibrosis (Fig.A), attenuated left ventricular remodeling (LVMM), and restored diastolic function (E/A ratio). Myocardial mitochondrial damage did not correlate with blood pressure but correlated directly with renal dysfunction (Fig.B).

Conclusion

Improved renal function by PTRA preserves myocardial mitochondria and enhances cardiac recovery regardless of RVH, underscoring reno-cardiac crosstalk in experimental MetS+RVH.

Funding

  • NIDDK Support