Evidence map›Paper›PMID 25480729›Full record

ReviewPediatric nephrology (Berlin, Germany)2015

Fibroblast growth factor 23 and acute kidney injury.

Javier A Neyra, Orson W Moe, Ming Chang Hu

Abstract readReview
In one paragraph

Review in Pediatric nephrology (Berlin, Germany), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. GALNT3 in Ischemia-Reperfusion Injury of the Kidney.Journal of the American Society of Nephrology : JASN · 2025
    Article
  3. Non-Classical Effects of FGF23: Molecular and Clinical Features.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Acute Kidney Injury and Pediatric Bone Health.Frontiers in pediatrics · 2020
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. 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

3 authors at 1 institution in 1 country.

Javier A NeyraDepartment of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX, 75390-885, USA.
Orson W MoeDepartment of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX, 75390-885, USA.
Ming Chang HuDepartment of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX, 75390-885, USA. ming-chang.hu@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · US

Funding

UT Southwestern O'Brien Kidney Research Core CenterP30DK079328 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MOE, ORSON W · 2007 to 2021
$16.9M
Klotho: Therapeutic Agent for Ischemia Reperfusion Induced Acute Kidney InjuryR01DK092461 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HU, MING-CHANG · 2011 to 2021
$3.7M
Klotho and Phosphate in Chronic Kidney Disease: Pathogenesis and TherapeuticsR01DK091392 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HU, MING-CHANG, MOE, ORSON W · 2011 to 2021
$3.2M
ENDOCRINE REGULATION OF MUSCLE GROWTH &DIFFERENTIATIONF32DK007938 · NIDDK · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI MCCUSKER, ROBERT H. · 1986 to 1987
–
NIDDK NIH HHS P30 DK079328NIDDK NIH HHS P30-DK-07938NIDDK NIH HHS R01 DK091392NIDDK NIH HHS R01-DK091392NIDDK NIH HHS R01 DK092461NIDDK NIH HHS R01-DK092461
6 · The paper itself

Abstract

Fibroblast growth factor 23 (FGF23), which is produced in bone, participates in the maintenance of phosphate metabolism and can serve as a biomarker for adverse cardiovascular outcomes in patients with chronic kidney disease and end-stage renal disease. Circulating FGF23 rapidly increases after acute kidney injury (AKI), preceding other known markers such as neutrophil gelatinase-associated lipocalin and serum creatinine. The increase in FGF23 in AKI appears to be independent of parathyroid hormone, vitamin D signaling pathways, and dietary phosphate. The potential mechanisms include: (1) increased production of FGF23 in the bone by yet-to-be-identified factors; (2) ectopic production of FGF23 by injured renal tubules; and (3) decreased renal clearance of circulating FGF23. Circulating FGF23 determined by intact FGF23 enzyme-linked immunosorbent assay (ELISA) is a more reliable biomarker of AKI than FGF23 C-terminal ELISA (a mixed readout of C-terminal fragment and intact FGF23). Given that FGF23 can be ectopically expressed in differentiated renal tubules and iron modulates FGF23 metabolism, an effect of iron on FGF23 expression in renal tubules is conceivable but remains to be confirmed. More clinical and experimental studies are required to validate the use of circulating FGF23 as a biomarker for the early identification of AKI and prediction of short- and long-term adverse outcomes post-AKI. More importantly, the biologic effect of increased FGF23 in AKI needs to be defined.

Indexed as

Acute Kidney InjuryBiomarkersFibroblast Growth Factor-23Fibroblast Growth FactorsHumansBiomarkersFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsAcute kidney injuryBoneFGF23IronKlotho

Identifiers

PMID25480729
PMCPMC4458234
OpenAlexW2063926600

What OpenQuestion holds

Textmetadata
LicenceTDM
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.