ArticleJournal of the American Society of Nephrology : JASN2019
Pharmacological Npt2a Inhibition Causes Phosphaturia and Reduces Plasma Phosphate in Mice with Normal and Reduced Kidney Function.
Article in Journal of the American Society of Nephrology : JASN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 44 citations in OpenAlex.
- Sex differences in renal acid-base regulation.Current opinion in nephrology and hypertension · 2026Review
- Renal Phosphate Reabsorption in Humans Depends on at Least Three Distinct Transporters Unlike in Mice.Acta physiologica (Oxford, England) · 2026Article
- Review
- Distinct roles of ferric carboxymaltose and ferric derisomaltose on phosphate homeostasis in iron deficiency anemia.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2025Article
- Sex differences in renal acid-base regulation.American journal of physiology. Renal physiology · 2025Article
- Genetic deletion of the sodium phosphate cotransporter NaPi2a ameliorates heart failure in mice.Scientific reports · 2025Article
- Phosphate in Physiological and Pathological Mineralization: Important yet Often Unheeded.MedComm · 2025Review
- Updates on renal phosphate transport.Current opinion in nephrology and hypertension · 2025Review
- Review
- Beyond SGLT2: proximal tubule transporters as potential drug targets for chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Review
- Genetic deletion of the kidney sodium/proton exchanger-3 (NHE3) does not alter calcium and phosphate balance due to compensatory responses.Kidney international · 2025Article
- Vitamin DScientific reports · 2024Article
- Pharmacology of Mammalian NaHandbook of experimental pharmacology · 2024Article
- Physiopathology of Phosphate Disorders.Advances in kidney disease and health · 2023Review
- Circadian clocks of the kidney: function, mechanism, and regulation.Physiological reviews · 2022Review
- NHE3 in the thick ascending limb is required for sustained but not acute furosemide-induced urinary acidification.American journal of physiology. Renal physiology · 2022Article
- Article
- Npt2a as a target for treating hyperphosphatemia.Biochemical Society transactions · 2022Review
- Enhanced phosphate absorption in intestinal epithelial cell-specific NHE3 knockout mice.Acta physiologica (Oxford, England) · 2022Article
- Fibroblast growth factor 23-Klotho and hypertension: experimental and clinical mechanisms.Pediatric nephrology (Berlin, Germany) · 2021Review
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6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe kidneys play an important role in phosphate homeostasis. Patients with CKD develop hyperphosphatemia in the later stages of the disease. Currently, treatment options are limited to dietary phosphate restriction and oral phosphate binders. The sodium-phosphate cotransporter Npt2a, which mediates a large proportion of phosphate reabsorption in the kidney, might be a good therapeutic target for new medications for hyperphosphatemia.
methodsThe authors assessed the effects of the first orally bioavailable Npt2a inhibitor (Npt2a-I) PF-06869206 in normal mice and mice that had undergone subtotal nephrectomy (5/6 Nx), a mouse model of CKD. Dose-response relationships of sodium, chloride, potassium, phosphate, and calcium excretion were assessed in response to the Npt2a inhibitor in both groups of mice. Expression and localization of Npt2a/c and levels of plasma phosphate, calcium, parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF-23) were studied up to 24-hours after Npt2a-I treatment.
resultsIn normal mice, Npt2a inhibition caused a dose-dependent increase in urinary phosphate (ED
conclusionsNpt2a inhibition causes a dose-dependent increase in phosphate, sodium and chloride excretion associated with reductions in plasma phosphate and PTH levels in normal mice and in a CKD mouse model.
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