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 X

Kidney Week

Abstract: SA-PO0431

Role of the Mineralocorticoid Receptor in Hemodialysis Vascular Access Dysfunction

Session Information

  • Dialysis: Vascular Access
    November 08, 2025 | Location: Exhibit Hall, Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Dialysis

  • 803 Dialysis: Vascular Access

Authors

  • Lee, Shina, Ewha Womans University Mokdong Hospital, Seoul, Korea (the Republic of)
  • Kim, Seung-Jung, Ewha Womans University Mokdong Hospital, Seoul, Korea (the Republic of)
Background

Vascular access stenosis is a major complication in dialysis patients, primarily occurring at the venous anastomosis site. While the role of the mineralocorticoid receptor (MR) has been well characterized in the heart and large arteries, its function in venous cells remains unclear. This study aims to investigate MR expression and activation pathways in venous endothelial cells (ECs) and smooth muscle cells (SMCs), and to evaluate the inhibitory effects of MR antagonists (MRAs).

Methods

Human umbilical vein endothelial cells (HUVECs) and venous SMCs were cultured and treated with the MR agonist aldosterone, as well as the MRAs spironolactone and finerenone. MR expression, SMC proliferation, oxidative stress, and inflammatory signaling pathways (MAPK, ERK1/2, NF-κB) were assessed by Western blot, RT-PCR, and ROS assays. The effects of pro-inflammatory stimuli (TNF-α) and the uremic toxin indoxyl sulfate on MR activation were also evaluated, along with the potential suppressive roles of MRAs and antioxidants (N-acetyl cysteine, probenecid).

Results

MR expression was upregulated in both HUVECs and SMCs upon aldosterone stimulation and was significantly suppressed by spironolactone and finerenone. MR activation was associated with increased SMC proliferation, oxidative stress, and activation of inflammatory pathways. TNF-α and indoxyl sulfate induced MR expression and inflammatory marker upregulation, which were attenuated by MRAs and antioxidants.

Conclusion

MR activation in venous ECs and SMCs promotes SMC proliferation, oxidative stress, and inflammation, contributing to vascular access stenosis. The non-steroidal MRA finerenone effectively attenuates these processes and may serve as a promising therapeutic strategy to prevent vascular access failure in dialysis patients.

Funding

  • Private Foundation Support

Digital Object Identifier (DOI)