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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.
Sulfate contributes to glycosaminoglycan structure and signaling. SLC26A1 mediates renal sulfate reabsorption in the proximal tubule. Mutations in humans are associated with severe hyposulfatemia due to renal sulfate wasting, reduced spine length, increased fracture risk, and decreased bone mineralization. We generated a mouse deficient for Slc26a1 to mimic the observations in humans.
To delete Slc26a1, we used CRISPR/Cas9 and confirmed deletion with PCR and immunoblotting. Plasma and urine sulfate levels were measured by turbidimetry. Bone structure, density, and distal-femur and L5 vertebral body mineralization were assessed with micro-computed tomography (µCT) and calcein-based bone histomorphometry. Safranin O staining and dimethylmethylene blue (DMMB) were used to analyze skeletal proteoglycan (PG) sulfation.
Slc26a1-null exhibited marked reduction in plasma sulfate associated with greatly increased fractional excretion of sulfate, confirming renal sulfate wasting. Bone histomorphometry showed impaired turnover, with double-labeled surfaces reduced by 51% in males and 44% in females (p < 0.01). Mineral apposition rate declined by 26% in females (p < 0.01) and 15% in males (n.s.), while bone formation rate was reduced by 38% in males (p < 0.001) and 33% in females (p < 0.01). Osteoblasts decreased 25% in males, (p < 0.01), with unchanged osteoclasts, female data pending. Safranin O staining confirmed reduced PG sulfation in KO mice. Saturation decreased 21% in males (p = 0.038) and 31% in females (p = 0.055, n.s.) in the growth plate, and 48% in males (p = 0.042) and 31% in females (p = 0.031) in bone, indicating defective sulfate incorporation. The DMMB assay further showed a 36% reduction in cartilage GAG sulfation (p < 0.05). µCT analysis revealed disturbed L5 trabecular architecture in males only, with vertebral connectivity density reduced by 24% (p < 0.01), and trabecular number by 7% (p < 0.01). Similarly, in the femur, bone volume was reduced by 13% (p < 0.05), connectivity density by 23% (p < 0.01), and apparent trabecular density by 17% (p < 0.01).
The Slc26a1-null mouse model links renal sulfate homeostasis to skeletal integrity. Our findings demonstrate the impact of the defective transporter on proteoglycan composition, cartilage structure, and bone mineralization.
This abstract was submitted and has been accepted at ASN Kidney Week 2025.
