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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
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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.
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Abstract titles should be brief and reflect the content of the abstract.
Cardiovascular disease (CVD) remains the leading cause of mortality in patients on maintenance hemodialysis (MHD). Vascular endothelial dysfunction (VED) is a critical initiating factor in CVD pathogenesis, where early intervention is essential to slow CVD progression. Sarcopenia, characterized by progressive loss of skeletal muscle mass and function, is common in MHD patients and closely associated with CVD development. Evidence suggests skeletal muscle may improve endothelial function and retard vascular aging through myokine secretion. Despite this protective potential, the association between sarcopenia and VED in MHD patients, as well as its underlying mechanisms, remains unclear. Thus, further investigation into this association is crucial for improving cardiovascular outcomes in this population.
We estimated genetic correlations between sarcopenia and VED traits using European GWAS data. Sarcopenia related traits included appendicular lean mass (ALM), walking pace, and low handgrip strength, while VED was assessed by soluble E-selectin (sE-selectin) and soluble vascular cell adhesion molecule-1 (sVCAM-1). Then we conducted a cross-sectional study in MHD patients at our center, in which VED was assessed by flow-mediated dilation (FMD). We employed linear regression to evaluate the association between sarcopenia and VED, supplemented by subgroup and restricted cubic spline (RCS) analyses to test robustness and nonlinearity.
In the genetic correlation analysis, both ALM and walking pace demonstrated significant negative correlations with sE-selectin levels (rg=-0.050 and rg=-0.232, respectively). Walking pace was also significantly negatively correlated with sVCAM-1 (rg=-0.156). In contrast, low handgrip strength shew no significant genetic correlations with either sE-selectin or sVCAM-1. In our cross-sectional study of 152 MHD patients, linear regression analysis identified that among the three diagnostic components of sarcopenia, only handgrip strength significantly associated with FMD. This association remained statistically significant after adjustment for gender, age, smoking, alcohol consumption, hypertension, diabetes, dialysis duration, lipid parameters, calcium, phosphorus, parathyroid hormone and albumin levels (β=0.267, 95% CI: 0.045–0.326, p=0.01). Subgroup analysis revealed that the positive association between the two remained consistent across subgroups stratified by age and diabetes history (p for interaction>0.05 for both). However, this association was modified by sex, remaining significant only in men (β=0.398, p<0.001) but not in women (β=-0.124, p=0.461). Furthermore, RCS analysis confirmed a linear positive relationship between handgrip strength and FMD in the elderly population (p for nonlinearity=0.298).
In summary, our findings point to a link between sarcopenia and VED in MHD patients, grounded in both genetic and clinical observations. The mechanistic drivers behind this connection, however, require our further investigation.
