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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 calcification is a major cause of cardiovascular morbidity in chronic kidney disease (CKD). Traditionally, medial calcification has been emphasized; however, recent evidence highlights intimal calcification within atherosclerotic plaques as a dominant and clinically relevant lesion. Hyperphosphatemia is strongly associated with calcification, yet the mechanisms linking phosphate excess to intimal mineralization remain unclear. Given that osteocytes sense phosphate through fibroblast growth factor receptor 1 (FGFR1), we hypothesized that neutrophils, which express FGFR1, mediate phosphate-induced calcification via neutrophil extracellular traps (NETs) and gasdermin D (GSDMD).
We performed in vitro assays using murine neutrophils to examine responses to elevated phosphate or calcium–phosphate crystals. NET formation was quantified by SYTOX green staining and CitH3 immunofluorescence. Pharmacological inhibitors targeting FGFR1, peptidylarginine deiminase 4 (PAD4), or GSDMD were applied to dissect signaling pathways. Proteomic profiling identified phosphate-responsive pathways. In vivo, an adenine plus high-phosphate diet was used to induce CKD-associated intimal vascular calcification in C57BL/6 mice. The effect of FGFR inhibition on vascular calcification and NET formation was evaluated by histology and immunohistochemistry.
High phosphate induced FGFR1-dependent NET formation in neutrophils, involving ERK phosphorylation, ROS production, and PAD4 activation. During this process, neutrophils degraded fetuin-A, an endogenous inhibitor of mineralization, thereby promoting calcium–phosphate crystallization. Formed crystals triggered secondary NET release through GSDMD activation, establishing a feed-forward loop that exacerbated vascular injury. Proteomic analyses revealed activation of proteasome- and oxidative stress–related pathways under high phosphate. In CKD mice (adenine and high phosphorus diet), intimal calcification was accompanied by neutrophil infiltration and NET formation. Pharmacological FGFR inhibition significantly reduced von Kossa–positive intimal lesions and CitH3 deposition without altering renal dysfunction, demonstrating a direct effect on vascular calcification.
These findings establish neutrophil activation via FGFR1 and GSDMD as central drivers of phosphate-induced intimal calcification in CKD. By linking hyperphosphatemia to immune-mediated vascular injury, our study highlights neutrophils as key amplifiers of the calcification process. Targeting the neutrophil FGFR1–GSDMD axis may represent a novel therapeutic strategy for reducing cardiovascular risk in CKD.
