Hemodialysis international. International Symposium on Home Hemodialysis · 2026
Tenapanor Beyond Phosphate: Gut Sodium Transport, Stool Transit Time, and Volume Balance in Dialysis Patients.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Corrêa Lucas Maciel de Almeida, Brandão Luiggi Kevin Virgino, Santiago Clara Belo Gamon, Barbosa Alexandre de Assis, Mazur Gabriel Rian, de Santana Gabriel Costa, Silva Yan Roberth Delmiro, Dante Letícia Esteves, Dutra Júnior Ivan Felipe
Аннотация
INTRODUCTION: Tenapanor, a minimally absorbed intestinal NHE3 inhibitor approved for hyperphosphatemia in dialysis, lowers phosphate and reduces intestinal sodium absorption. Its sodium-water signal may have implications beyond phosphate but remains poorly separated from diarrhea-mediated losses and dialysis prescription artifacts.
METHODS: This perspective synthesizes pharmacologic, trial, dialysis physiology, and CKD-MBD evidence to propose a hypothesis-generating framework for evaluating tenapanor beyond serum phosphate. We focused on intestinal sodium handling, stool transit, interdialytic weight gain, ultrafiltration stress, hemodynamic tolerance, and fibroblast growth factor 23.
FINDINGS: Tenapanor-associated diarrhea and modest serum sodium reduction should be interpreted not only as tolerability events but also as potential markers of on-target intestinal sodium-water modulation. In selected phenotypes, reduced effective sodium loading could theoretically attenuate thirst, lower interdialytic weight gain, and reduce ultrafiltration demand; in others, diarrhea-mediated losses could worsen hypovolemia or intradialytic instability. Tenapanor-induced fibroblast growth factor 23 reduction is biologically plausible but remains an unvalidated bridge to cardiovascular or patient-centered outcomes.
DISCUSSION: Future studies should prospectively distinguish sodium-volume benefit from gastrointestinal intolerance using standardized dialysis endpoints, stool metrics, dialysate sodium data, bioimpedance, and imaging or patient-centered outcomes. Tenapanor should therefore be studied as an intestinal sodium-phosphate-volume intervention, not merely a phosphate-lowering drug.
METHODS: This perspective synthesizes pharmacologic, trial, dialysis physiology, and CKD-MBD evidence to propose a hypothesis-generating framework for evaluating tenapanor beyond serum phosphate. We focused on intestinal sodium handling, stool transit, interdialytic weight gain, ultrafiltration stress, hemodynamic tolerance, and fibroblast growth factor 23.
FINDINGS: Tenapanor-associated diarrhea and modest serum sodium reduction should be interpreted not only as tolerability events but also as potential markers of on-target intestinal sodium-water modulation. In selected phenotypes, reduced effective sodium loading could theoretically attenuate thirst, lower interdialytic weight gain, and reduce ultrafiltration demand; in others, diarrhea-mediated losses could worsen hypovolemia or intradialytic instability. Tenapanor-induced fibroblast growth factor 23 reduction is biologically plausible but remains an unvalidated bridge to cardiovascular or patient-centered outcomes.
DISCUSSION: Future studies should prospectively distinguish sodium-volume benefit from gastrointestinal intolerance using standardized dialysis endpoints, stool metrics, dialysate sodium data, bioimpedance, and imaging or patient-centered outcomes. Tenapanor should therefore be studied as an intestinal sodium-phosphate-volume intervention, not merely a phosphate-lowering drug.