Evidence map›Paper›PMID 21346724›Full record

ReviewKidney international. Supplement2011

Phosphate and FGF-23.

Harald Jüppner

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Kidney international. Supplement, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07171216 (The Effect of REgulation of PArathyroId hoRmone in Patients With Chronic Kidney Disease to Investigate the Change in Bone Mineral Density), which is not on this map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
10.1field-weighted citation impact, top 1% 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.

NCT07171216 narecruitingnot on this mapstarted 2025, after this paper: background citation

The Effect of REgulation of PArathyroId hoRmone in Patients With Chronic Kidney Disease to Investigate the Change in Bone Mineral Density (Biskjoldbruskkirtelhormon og knogletæthed Hos Patienter Med Kronisk Nyresygdom)

TypeinterventionalSponsorHerlev HospitalRan2025 to 2027Enrolled70ConditionsChronic Kidney Disease Mineral and Bone DisorderArmsTreat to target
3 · Its place in the literature

Who cites it

64 citing papers in PubMed, 186 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Vitamin DScientific reports · 2024
    Article
  14. Review
  15. Article
  16. Article
  17. Observational
  18. Review
  19. Mineral Bone Disorders in Kidney Disease Patients: The Ever-Current Topic.International journal of molecular sciences · 2022
    Review
  20. Applications of Metabolomics in Calcium Metabolism Disorders in Humans.International journal of molecular sciences · 2022
    Review

4 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Harald JüppnerEndocrine Unit and Pediatric Nephrology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA. hjueppner@partners.org
Massachusetts General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factor (FGF)-23 is probably the most important regulator of serum phosphate and calcitriol (1,25(OH)₂D₃) levels. It is secreted by osteocytes and osteoblasts in response to oral phosphate loading or increased serum 1,25(OH)₂D₃ levels. In human chronic kidney disease (CKD), plasma FGF-23 appears to be a sensitive biomarker of abnormal renal phosphate handling, as FGF-23 levels increase during early stages of kidney malfunction. In humans and animals with CKD, elevated FGF-23 levels increase fractional phosphate excretion, reduce serum phosphate levels, and reduce 1α-hydroxylase activity, which reduces 1,25(OH)₂D₃ formation thereby increasing parathyroid hormone (PTH) secretion. FGF-23 thus has a key adaptive role in maintaining normophosphatemia. Plasma FGF-23 continues to increase as CKD progresses, increasing by orders of magnitude in end-stage renal disease. At the same time, responsiveness to FGF-23 declines as the number of intact nephrons declines, which is associated with reduced expression of Klotho, the co-receptor required for FGF-23 signaling. In late CKD, FGF-23 cannot reduce serum phosphate levels, and abnormally high plasma FGF-23 concentrations appear to exert unwarranted off-target effects, including left ventricular hypertrophy, faster CKD progression, and premature mortality. Lowering serum phosphate levels through the use of oral phosphate binders and/or long-acting PTH agents may reduce FGF-23 levels in early CKD stages, thereby limiting off-target effects, which may improve patient outcomes.

Indexed as

Bone DiseasesCalciumChronic DiseaseDisease ProgressionFibroblast Growth Factor-23Fibroblast Growth FactorsHumansKidney DiseasesPhosphatesCalciumFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsPhosphates

Identifiers

PMID21346724
PMCPMC3257051
OpenAlexW2061453367

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.