Evidence map›Paper›PMID 26864938›Full record

ReviewAmerican journal of physiology. Renal physiology2016

FGF23 from bench to bedside.

Csaba P Kovesdy, L Darryl Quarles

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 63 citations in OpenAlex.

  1. Angiotensin-related genetic determinants of cardiovascular disease in patients undergoing hemodialysis.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2019
    Trial
  2. Review
  3. Article
  4. Review
  5. Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024
    Review
  6. Review
  7. Renal Clearance of Fibroblast Growth Factor-23 (FGF23) and its Fragments in Humans.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. FGF23 signalling and physiology.Journal of molecular endocrinology · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Csaba P KovesdyUniversity of Tennessee Health Science Center, Memphis, Tennessee; and Memphis Veterans Affairs Medical Center, Memphis, Tennessee ckovesdy@uthsc.edu.
L Darryl QuarlesUniversity of Tennessee Health Science Center, Memphis, Tennessee; and.
Memphis VA Medical Center · USUniversity of Tennessee Health Science Center · US

Funding

Regulation and Function of FGF23R01AR045955 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI QUARLES, L DARRYL · 1999 to 2016
$4.8M
NIAMS NIH HHS R01 AR045955
6 · The paper itself

Abstract

There is a strong association between elevated circulating fibroblast growth factor-23 (FGF23) levels and adverse outcomes in patients with chronic kidney disease (CKD) of all stages. Initially discovered as a regulator of phosphate and vitamin D homeostasis, FGF23 has now been implicated in several pathophysiological mechanisms that may negatively impact the cardiovascular and renal systems. FGF23 is purported to have direct (off-target) effects in the myocardium, as well as canonical effects on FGF receptor/α-klotho receptor complexes in the kidney to activate the renin-angiotensin-aldosterone system, modulate soluble α-klotho levels, and increase sodium retention, to cause left ventricular hypertrophy (LVH). Conversely, FGF23 could be an innocent bystander produced in response to chronic inflammation or other processes associated with CKD that cause LVH and adverse cardiovascular outcomes. Further exploration of these complex mechanisms is needed before modulation of FGF23 can become a legitimate clinical target in CKD.

Indexed as

AnimalsBiomarkersFibroblast Growth Factor-23Fibroblast Growth FactorsHumansPrognosisRenal Insufficiency, ChronicBiomarkersFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth Factorsboneheartkidney

Identifiers

PMID26864938
PMCPMC6425620
OpenAlexW2294844169

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.