Abstract: TH-PO0222
Role of Tenapanor in the Management of Hyperphosphatemia in Patients with Kidney Failure (KF) Undergoing Peritoneal Dialysis (PD): Real-World Experience from a Single Center
Session Information
- Bone and Mineral Metabolism: Clinical Reports and Practice
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Authors
- Raju, Swetha, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Pope, Donna E., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Saxena, Ramesh, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Background
Hyperphosphatemia contributes to increased cardiovascular risk, and mortality in KF. Traditional phosphate binders are often limited by high pill burden, gastrointestinal side effects, and suboptimal adherence. Recently, tenapanor, a first-in-class intestinal phosphate absorption inhibitor has shown promising results in hypherphosphatemia management.
Methods
In this prospective observational study, we evaluated the efficacy and safety of tenapanor in KF patients on peritoneal dialysis (PD) at our center. Patients with persistent hyperphosphatemia for ≥3 months despite phosphate binders were considered for tenapanor between September 1, 2024, and January 2025. Follow-up continued until death, transition to hemodialysis (HD), kidney transplantation, or the end of study period (April 30, 2025). Primary goals included: 1) Mean change in serum phosphate from baseline; 2) Number of patients with phosphate reduction; 3) Incidence of adverse events.
Results
Of 28 eligible patients, 2 were denied insurance coverage, 1 declined treatment, and 12 discontinued within a week due to adverse events, primarily diarrhea. 13 patients (5 males, 8 females; mean age 53.84 years) continued tenapanor. Mean starting dose was 52.3 mg/day; 11 maintained the starting dose, while 2 reduced it due to poor tolerance. Mean baseline serum phosphate was 7.73 mg/dL. During follow-up (mean 4.38 months), 1 patient expired, 1 underwent transplantation, and 2 transitioned to HD. End-of-study mean serum phosphate was 7.1 mg/dL, with a modest mean reduction of 0.23 mg/dL. Only 5 of 13 patients showed improvement; 8 had higher phosphate levels at study end. Diarrhea or loose stools occurred in 7 patients, and 4 required dose reductions.
Conclusion
In this real-world study, tenapanor did not result in significant phosphate reduction over a mean 4.38 month follow-up. Only 5 of 13 patients showed improvement, and gastrointersinal side effects were common, leading to dose reductions or discontinuation. Over half of eligible patients were unable to initiate or continue therapy, mainly due to diarrhea. Larger, multicenter studies with longer follow-up are needed to further explore the safety and efficacy of tenapanor’s role in phosphate control for PD patients.