Evidence map›Paper›PMID 23179196›Full record

ReviewPediatric nephrology (Berlin, Germany)2013

Hypophosphatemia and growth.

Fernando Santos, Rocío Fuente, Natalia Mejia, Laura Mantecon, Helena Gil-Peña, Flor A Ordoñez

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Observational
  3. Switching from active vitamin D and phosphate supplementation to burosumab significantly corrects lower limb malalignment in pediatric X-linked hypophosphatemia.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025
    Observational
  4. Real-world effectiveness of burosumab vs oral phosphate and active vitamin D in adults with X-linked hypophosphatemia.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025
    Observational
  5. Article
  6. Review
  7. Observational
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. X-Linked Hypophosphatemia: A New Era in Management.Journal of the Endocrine Society · 2020
    Review
  18. Article
  19. Article
  20. Functional analysis of aBone & joint research · 2019
    Article
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

6 authors at 2 institutions in 1 country.

Fernando SantosHospital Universitario Central de Asturias & University of Oviedo, Oviedo, Asturias, Spain. fsantos@uniovi.es
Rocío Fuente
Natalia Mejia
Laura Mantecon
Helena Gil-Peña
Flor A Ordoñez
Universidad de Oviedo · ESHospital Universitario Central de Asturias · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the last decade the discovery of fibroblast growth factor 23 (FGF23) and the progressive and ongoing clarification of its role in phosphate and mineral metabolism have led to expansion of the diagnostic spectrum of primary hypophosphatemic syndromes. This article focuses on the impairment of growth in these syndromes. Growth retardation is a common, but not constant, feature and it presents with large variability. As a result of the very low prevalence of other forms of primary hypophosphatemic syndromes, the description of longitudinal growth and the pathogenesis of its impairment have been mostly studied in X-linked hypophosphatemia (XLH) patients and in Hyp mice, the animal model of this disease. In general, children with XLH have short stature with greater shortness of lower limbs than trunk. Treatment with phosphate supplements and 1α vitamin D derivatives heals active lesions of rickets, but does not normalize growth of XLH patients. Patients might benefit from recombinant human growth hormone (rhGH) therapy, which may accelerate the growth rate without increasing body disproportion or correcting hypophosphatemia. These clinical data as well as research findings obtained in Hyp mice suggest that the pathogenesis of defective growth in XLH and other hypophosphatemic syndromes is not entirely dependent on the mineralization disorder and point to other effects of hypophosphatemia itself or FGF23 on the metabolism of bone and growth plate.

Indexed as

Body HeightBone DevelopmentGenetic Diseases, X-LinkedAnimalsBone and BonesDietary SupplementsDisease Models, AnimalFamilial Hypophosphatemic RicketsFibroblast Growth Factor-23Fibroblast Growth FactorsGrowth DisordersHuman Growth HormoneHumansMiceMice, TransgenicPHEX Phosphate Regulating Neutral EndopeptidaseFGF23 protein, humanFgf23 protein, mouseFibroblast Growth Factor-23Fibroblast Growth FactorsHuman Growth HormonePHEX Phosphate Regulating Neutral EndopeptidasePhex protein, mousePhosphatesRecombinant ProteinsVitamins

Identifiers

PMID23179196
OpenAlexW2066145596

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.