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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.
Calciphylaxis is a rare, life-threatening condition primarily affecting end-stage kidney disease(ESKD) patients, characterized by painful skin ulcers, necrosis, and high mortality. Pathologically, it involves microvascular calcification, intimal fibroplasia, and thrombosis. Its pathogenesis remains unclear, and effective treatments are lacking.
We report a 49-year-old uremic woman with progressive left lower-limb ulcers, severe pain, and black eschar since December 2024. Diagnosis was confirmed by skin biopsy. After failing conventional therapy, she received intravenous and subcutaneous human amniotic-derived mesenchymal stem cells (hAMSCs). Over six months, infection markers, biochemical parameters, and bone metabolism were monitored. Wound healing was assessed using the Bates-Jensen Wound Assessment Tool for Calcific Uremic Arteriolopathy (BWAT-CUA); pain was measured via the Visual Analogue Scale (VAS) . Serial skin biopsies were analyzed with H&E, alizarin red, and Von Kossa staining. Ultrastructural changes were evaluated by transmission and scanning electron microscopy.
Post-hAMSC treatment, wound healing progressed with soft tissue regeneration. BWAT-CUA score improved from 35 (baseline) to 11 (1 week), then 8 (1–6 months). VAS pain score dropped from 100 to 0 by six months (Fig 1).
Inflammatory markers declined, albumin increased, and calcium, phosphorus, and PTH remained within normal ranges (Fig 2).
Pre-treatment biopsies showed occluded arterioles, inflammatory infiltration, nerve edema, and medial calcification (confirmed by alizarin red and Von Kossa). Electron microscopy revealed endothelial swelling, luminal debris, and tissue damage. One week post-treatment, H&E showed granulation tissue, angiogenesis, and reduced inflammation; calcium deposits decreased. Ultrastructure revealed improved tissue architecture and neovascularization. By one month, epidermal and dermal regeneration, mature neovessels, and minimal calcification were observed. Organelle abnormalities and edema resolved. At three months, skin structure was fully restored, with no inflammation in ganglion cells; endothelial ultrastructure normalized (Fig 3).
hAMSC therapy markedly improved wound healing in calciphylaxis. Histological and ultrastructural improvements—angiogenesis, reduced inflammation, and decreased calcification—appeared within one week. By one month, tissue remodeling was evident; by three months, skin and vascular architecture were nearly restored. hAMSCs likely act via promoting vascular regeneration, modulating inflammation, and inhibiting calcification, supporting their potential as a regenerative therapy for calciphylaxis.
