Evidence map›Paper›PMID 30353318›Full record

ReviewCurrent osteoporosis reports2018

Non-renal-Related Mechanisms of FGF23 Pathophysiology.

Mark R Hanudel, Marciana Laster, Isidro B Salusky

Abstract readReview
In one paragraph

Review in Current osteoporosis reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Jansen's Disease: Bone Abnormalities Beyond Chondrodysplasia.The Journal of clinical endocrinology and metabolism · 2025
    Article
  2. Review
  3. Associations between anemia and FGF23 in the CKiD study.Pediatric nephrology (Berlin, Germany) · 2024
    Article
  4. Review
  5. Review
  6. Hypoxia-Inducible Factors Signaling in Osteogenesis and Skeletal Repair.International journal of molecular sciences · 2022
    Review
  7. Two long-term phase 3 studies of enarodustat (JTZ-951) in Japanese anemic patients with chronic kidney disease not on dialysis or on maintenance hemodialysis: SYMPHONY ND-Long and HD-Long studies.Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Association of increased renalJournal of clinical biochemistry and nutrition · 2020
    Article
  12. Review
  13. Review
  14. 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.

Mark R HanudelUCLA Department of Pediatrics, Division of Pediatric Nephrology, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, MDCC A2-383, Los Angeles, CA, 90095-1752, USA. mhanudel@mednet.ucla.edu.
Marciana LasterUCLA Department of Pediatrics, Division of Pediatric Nephrology, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, MDCC A2-383, Los Angeles, CA, 90095-1752, USA.
Isidro B SaluskyUCLA Department of Pediatrics, Division of Pediatric Nephrology, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, MDCC A2-383, Los Angeles, CA, 90095-1752, USA.
University of California, Los Angeles · US

Funding

Translational Research Training in Pediatric NephrologyT32DK104687 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SALUSKY, ISIDRO B. · 2015 to 2019
$879k
Regulation of Fibroblast Growth Factor 23 by Iron and Anemia in Chronic Kidney DiseaseK08DK111980 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HANUDEL, MARK ROBERT · 2016 to 2019
$758k
NIDDK NIH HHS K08 DK111980NIDDK NIH HHS T32 DK104687
6 · The paper itself

Abstract

purpose of reviewWe will review non-renal-related mechanisms of fibroblast growth factor 23 (FGF23) pathophysiology. RECENT

findingsFGF23 production and metabolism may be affected by many bone, mineral, and kidney factors. However, it has recently been demonstrated that other factors, such as iron status, erythropoietin, and inflammation, also affect FGF23 production and metabolism. As these non-mineral factors are especially relevant in the setting of chronic kidney disease (CKD), they may represent emerging determinants of CKD-associated elevated FGF23 levels. Moreover, FGF23 itself may promote anemia and inflammation, thus contributing to the multifactorial etiologies of these CKD-associated comorbidities. CKD-relevant, non-mineral-related, bidirectional relationships exist between FGF23 and anemia, and between FGF23 and inflammation. Iron deficiency, anemia, and inflammation affect FGF23 production and metabolism, and FGF23 itself may contribute to anemia and inflammation, highlighting complex interactions that may affect aspects of CKD pathogenesis and treatment.

Indexed as

Bone and BonesBone Diseases, MetabolicFibroblast Growth Factor-23Fibroblast Growth FactorsHumansRenal Insufficiency, ChronicFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsAnemiaChronic kidney diseaseCKD-mineral and bone disorderFibroblast growth factor 23Iron

Identifiers

PMID30353318
PMCPMC6234055
OpenAlexW2896719825

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.