ReviewCurrent opinion in nephrology and hypertension2025
Updates on renal phosphate transport.
Review in Current opinion in nephrology and hypertension, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed.
- Review
- Study on metabolic differences and microbiota distribution in patients with infection-induced kidney stones by gender.BMC microbiology · 2026Article
- The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026Review
- Targeting Hypercalciuria in SLC34A1-Related Disorders: Impact of Oral Phosphate Therapy and Novel Genetic Insights in Pediatric Case Series.Calcified tissue international · 2026Article
- Identification of a Novel HomozygousInternational journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewThe kidneys control systemic phosphate balance by regulating phosphate transporters mediating the reabsorption of inorganic phosphate (Pi). At least three different Na + -driven Pi cotransporters are located in the brush border membrane (BBM) of proximal tubule cells, NaPi-IIa (SLC34A1), NaPi-IIc (SLC34A3) and PiT-2 (SLC20A2). This review will discuss novel aspects of their regulation, pharmacology, and genetics. RECENT
findingsRenal NaPi transporters are not only acutely regulated by the phosphaturic hormones parathyroid hormone (PTH) and Fibroblast Growth Factor 23 (FGF23) but possibly also by further mechanisms. A role of inositol hexakisphosphate (IP6) kinases has been found and their deletion from kidneys causes hypophosphatemia, hyperphosphaturia, and bone demineralization. Inhibitors of NaPis elicit phosphaturia and may reduce levels of PTH and FGF23 in chronic kidney disease (CKD) models. The relevance of renal NaPi transporters is highlighted by loss-of-function mutations in SLC34 transporters and analysis of patients provides new insights into diseases caused by variants. Major manifestations include nephrocalcinosis and -lithiasis, rickets, and variants may predispose to an accelerated decline in kidney function. SUMMARY: Renal Pi transporters are regulated, may provide novel drug targets for prevention or treatment of hyperphosphatemia, and contribute to the genetic risk to develop kidney stones and CKD.
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