ReviewDrugs2018
Targeting Gastrointestinal Transport Proteins to Control Hyperphosphatemia in Chronic Kidney Disease.
Review in Drugs, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Pharmacokinetics, Safety, and Tolerability of Tenapanor in Healthy Chinese and Caucasian Volunteers: A Randomized, Open-Label, Single-Center, Placebo-Controlled Phase 1 Study.International journal of clinical practice · 2024Trial
- Modified-release nicotinamide for the treatment of hyperphosphataemia in haemodialysis patients: 52-week efficacy and safety results of the phase 3 randomized controlled NOPHOS trial.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023Trial
- Safety and Efficacy of Tenapanor for Long-term Serum Phosphate Control in Maintenance Dialysis: A 52-Week Randomized Phase 3 Trial (PHREEDOM).Kidney360 · 2021Trial
- Targeting cardiovascular and metabolic risk modification in end stage renal disease (ESRD): a randomized controlled clinical trial on niacin's effects on lipoprotein(a) and biochemical markers in hemodialysis patients.Frontiers in medicine · 2025Article
- Effects of pharmacological inhibition of the sodium-dependent phosphate cotransporter 2b (NPT2b) on intestinal phosphate absorption in mouse and rat models.Pharmacology research & perspectives · 2022Article
- Sucroferric oxyhydroxide for hyperphosphatemia: a review of real-world evidence.Journal of nephrology · 2022Review
- Contribution of Gut Microbiota-Derived Uremic Toxins to the Cardiovascular System Mineralization.Toxins · 2021Review
- NaPi-IIb Inhibition for Hyperphosphatemia in CKD Hemodialysis Patients.Kidney international reports · 2021Article
- Dietary Phosphorus as a Marker of Mineral Metabolism and Progression of Diabetic Kidney Disease.Nutrients · 2021Review
- Uremic Vascular Calcification: The Pathogenic Roles and Gastrointestinal Decontamination of Uremic Toxins.Toxins · 2020Review
- Tenapanor: First Approval.Drugs · 2019Review
- Clinical aspects of the phosphate transporters NaPi-IIa and NaPi-IIb: mutations and disease associations.Pflugers Archiv : European journal of physiology · 2019Review
- Phosphate Absorption and Hyperphosphatemia Management in Kidney Disease: A Physiology-Based Review.Kidney medicineReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Management of hyperphosphatemia in patients with dialysis-dependent chronic kidney disease remains a major challenge, requiring a multifaceted approach that includes dietary phosphate restriction, dialysis, and phosphate binders. However, these treatments fail to meet serum phosphate targets in many patients, potentially further exacerbating the significant morbidity and mortality burden associated with the disease. Recent advances in our understanding of the mechanisms underlying phosphate homeostasis have shed new light on the issue and suggest that gastrointestinal transport proteins may be promising targets for new hyperphosphatemia treatments. Drugs that inhibit or downregulate these transport proteins, and thus reduce phosphate uptake from the gut, may overcome some of the limitations of existing phosphate-lowering strategies, such as interdialytic rises in serum phosphate levels, poor adherence to dietary and phosphate-binder regimens, and maladaptive responses that can increase gastrointestinal phosphate absorption. Here, we review the latest preclinical and clinical data for two candidates in this novel drug class: tenapanor, a small-molecule inhibitor of the sodium/hydrogen ion-exchanger isoform 3, and nicotinamide, an inhibitor of sodium-phosphate-2b cotransporters. We also discuss how potential synergies in their mechanisms of action suggest that coadministering phosphate binders with sodium-phosphate-2b cotransporter inhibitors may yield additive benefits over traditional phosphate-binder therapy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.