Evidence map›Paper›PMID 22859851›Full record

ArticleJournal of the American Society of Nephrology : JASN2012

Npt2b deletion attenuates hyperphosphatemia associated with CKD.

Susan C Schiavi, Wen Tang, Christina Bracken, Stephen P O'Brien, Wenping Song, Joseph Boulanger, Susan Ryan, Lucy Phillips, Shiguang Liu, Cynthia Arbeeny and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Npt2a as a target for treating hyperphosphatemia.Biochemical Society transactions · 2022
    Review
  16. Article
  17. Phosphate Balance and CKD-Mineral Bone Disease.Kidney international reports · 2021
    Review
  18. Article
  19. Review
  20. Novel Treatments from Inhibition of the Intestinal Sodium-Hydrogen Exchanger 3.International journal of nephrology and renovascular disease · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Susan C SchiaviThe Sanofi-Genzyme R&D Center, 49 New York Avenue, Framingham, MA 01701-9322, USA. susan.schiavi@genzyme.com
Wen Tang
Christina Bracken
Stephen P O'Brien
Wenping Song
Joseph Boulanger
Susan Ryan
Lucy Phillips
Shiguang Liu
Cynthia Arbeeny
Steven Ledbetter
Yves Sabbagh
Genesys (United States) · USSanofi (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of cardiovascular events and mortality strongly correlates with serum phosphate in individuals with CKD. The Npt2b transporter contributes to maintaining phosphate homeostasis in the setting of normal renal function, but its role in CKD-associated hyperphosphatemia is not well understood. Here, we used adenine to induce uremia in both Npt2b-deficient and wild-type mice. Compared with wild-type uremic mice, Npt2b-deficient uremic mice had significantly lower levels of serum phosphate and attenuation of FGF23. Treating Npt2b-deficient mice with the phosphate binder sevelamer carbonate further reduced serum phosphate levels. Uremic mice exhibited high turnover renal osteodystrophy; treatment with sevelamer significantly decreased the number of osteoclasts and the rate of mineral apposition in Npt2b-deficient mice, but sevelamer did not affect bone formation and rate of mineral apposition in wild-type mice. Taken together, these data suggest that targeting Npt2b in addition to using dietary phosphorus binders may be a therapeutic approach to modulate serum phosphate in CKD.

Indexed as

AnimalsChronic Kidney Disease-Mineral and Bone DisorderDisease Models, AnimalFibroblast Growth Factor-23Fibroblast Growth FactorsHumansHyperphosphatemiaMiceMice, KnockoutPolyaminesRenal Insufficiency, ChronicSevelamerSodium-Phosphate Cotransporter Proteins, Type IIbUremiaFGF23 protein, humanFgf23 protein, mouseFibroblast Growth Factor-23Fibroblast Growth FactorsPolyaminesSevelamerSlc34a2 protein, mouseSodium-Phosphate Cotransporter Proteins, Type IIb

Identifiers

PMID22859851
PMCPMC3458457
OpenAlexW2159814168

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.