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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
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).
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). Additionally, a chronic kidney disease (CKD) mouse model underwent arteriovenous fistula (AVF) surgery to evaluate the in vivo effects of finerenone on vascular access stenosis. Mice were orally treated with finerenone before and after AVF surgery, and vascular tissues were analyzed histologically and molecularly.
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. In the CKD mouse model, finerenone treatment reduced AVF stenosis and suppressed expression of MR and inflammation/fibrosis-related markers (TNF-α, MCP-1, ICAM-1, VCAM-1).
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.
