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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.
Hyperphosphatemia in renal failure is associated with vascular calcification and increased cardiovascular mortality. Although the intestine is the primary site of phosphate entry into the body, the molecular mechanisms governing intestinal phosphate absorption remain incompletely understood. Phosphate absorption occurs via transcellular pathways (mediated by NaPi-IIb) and paracellular pathways (through tight junctions). Under modern high-phosphate dietary conditions, the paracellular route predominates. Paracellular transport comprises two mechanisms: the claudin composition-dependent "pore" pathway (assessed by TEER) and the dynamically regulated "leak" pathway (evaluated by macromolecular permeability). This study investigated the molecular mechanisms underlying paracellular phosphate absorption.
Male Wistar rats (12 weeks old, n=5/group) received oral tenapanor (NHE3 inhibitor) or vehicle for 2 days. Serum, fecal, and urinary phosphate levels were measured. Jejunal epithelial cells were analyzed for claudin and myosin light chain 2 (MLC2) expression by Western blotting and immunofluorescence. Wild-type and claudin-1, -2, -3, -4, -7-deficient (quintuple knockout; quinKO) MDCK cells were treated with tenapanor to assess TEER and phosphate permeability changes.
Tenapanor increased fecal phosphate excretion without altering serum phosphate in rats with normal renal and bone metabolism, confirming intestinal absorption inhibition. In jejunal epithelial cells, tenapanor reduced MLC2 protein levels while claudin levels remained unchanged. In wild-type MDCK cells, tenapanor decreased TEER yet did not alter phosphate permeability. QuinKO cells showed constitutively low TEER and no response to tenapanor in either TEER or phosphate permeability, indicating claudin-dependent tenapanor effects.
Tenapanor-mediated phosphate absorption inhibition correlates with reduced MLC2 expression in jejunal epithelium, suggesting modulation of actomyosin-dependent paracellular dynamics. The dissociation between TEER changes and phosphate permeability indicates that phosphate primarily transits via the "leak" pathway rather than the claudin-selective "pore" pathway. These findings help to establish a mechanistic framework for therapeutic targeting of paracellular phosphate transport in hyperphosphatemia management.
