Evidence map›Paper›PMID 23698235›Full record

ArticleKidney international2013

Dietary phosphate restriction suppresses phosphaturia but does not prevent FGF23 elevation in a mouse model of chronic kidney disease.

Shiqin Zhang, Ryan Gillihan, Nan He, Timothy Fields, Shiguang Liu, Troy Green, Jason R Stubbs

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. Article
  3. The effects of elevated phosphate on the kidney - damaging the gatekeeper.Pflugers Archiv : European journal of physiology · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Phosphate as a Signaling Molecule.Calcified tissue international · 2021
    Review
  8. Dietary phosphate restriction attenuates polycystic kidney disease in mice.American journal of physiology. Renal physiology · 2020
    Article
  9. Fibroblast growth factor 23 and α-Klotho co-dependent and independent functions.Current opinion in nephrology and hypertension · 2019
    Review
  10. Review
  11. Review
  12. Spleen contributes significantly to increased circulating levels of fibroblast growth factor 23 in response to lipopolysaccharide-induced inflammation.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017
    Article
  13. Multiple faces of fibroblast growth factor-23.Current opinion in nephrology and hypertension · 2016
    Review
  14. Article
  15. Article
  16. Article
  17. The use of fibroblast growth factor 23 testing in patients with kidney disease.Clinical journal of the American Society of Nephrology : CJASN · 2014
    Review
  18. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Shiqin ZhangThe Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas, USA.
Ryan Gillihan
Nan He
Timothy Fields
Shiguang Liu
Troy Green
Jason R Stubbs
University of Kansas Medical Center · US

Funding

Exploring the interrelationships of mineral metabolism pathways in kidney diseaseK08DK087949 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI STUBBS, JASON · 2010 to 2014
$757k
NIDDK NIH HHS K08 DK087949NIDDK NIH HHS K08-DK087949
6 · The paper itself

Abstract

Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone that in end-stage renal disease is markedly increased in serum; however, the mechanisms responsible for this increase are unclear. Here, we tested whether phosphate retention in chronic kidney disease (CKD) is responsible for the elevation of FGF23 in serum using Col4α3 knockout mice, a murine model of Alport disease exhibiting CKD. We found a significant elevation in serum FGF23 in progressively azotemic 8- and 12-week-old CKD mice along with an increased fractional excretion of phosphorus. Both moderate and severe phosphate restriction reduced fractional excretion of phosphorus by 8 weeks, yet serum FGF23 levels remained strikingly elevated. By 12 weeks, FGF23 levels were further increased with moderate phosphate restriction, while severe phosphate restriction led to severe bone mineralization defects and decreased FGF23 production in bone. CKD mice on a control diet had low serum 1,25-dihydroxyvitamin D (1,25(OH)(2)D) levels and 3-fold higher renal Cyp24α1 gene expression compared to wild-type mice. Severe phosphate restriction increased 1,25(OH)(2)D levels in CKD mice by 8 weeks and lowered renal Cyp24α1 gene expression despite persistently elevated serum FGF23. Renal klotho gene expression declined in CKD mice on a control diet, but improved with severe phosphate restriction. Thus, dietary phosphate restriction reduces the fractional excretion of phosphorus independent of serum FGF23 levels in mice with CKD.

Indexed as

25-Hydroxyvitamin D3 1-alpha-HydroxylaseAdministration, OralAnimalsAutoantigensBone and BonesCollagen Type IVDisease Models, AnimalFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseHypophosphatemia, FamilialKidneyKlotho ProteinsMaleMice1,25-dihydroxyvitamin D25-Hydroxyvitamin D3 1-alpha-HydroxylaseAutoantigensCollagen Type IVFgf23 protein, mouseFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseKlotho ProteinsPhosphatesSteroid Hydroxylasestype IV collagen alpha3 chainVitamin DVitamin D3 24-Hydroxylase

Identifiers

PMID23698235
PMCPMC3758787
OpenAlexW1970701220

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Registered trials

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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.