Evidence map›Paper›PMID 22622492›Full record

ReviewKidney international2012

Update on fibroblast growth factor 23 in chronic kidney disease.

Myles Wolf

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed, 2 pooled it
22.1field-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.

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

180 citing papers in PubMed, 2 syntheses or guidelines pooled it, 380 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  6. Effect of ferric citrate on serum phosphate and fibroblast growth factor 23 among patients with nondialysis-dependent chronic kidney disease: path analyses.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2019
    Trial
  7. The effects of tenapanor on serum fibroblast growth factor 23 in patients receiving hemodialysis with hyperphosphatemia.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2019
    Trial
  8. Trial
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  12. Ferric citrate hydrate for the treatment of hyperphosphatemia in nondialysis-dependent CKD.Clinical journal of the American Society of Nephrology : CJASN · 2014
    Trial
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  17. Observational
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  20. Review

120 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.

Myles WolfDepartment of Medicine, Division of Nephrology and Hypertension, University of Miami Miller School of Medicine, Miami, Florida 33136, USA.
University of Miami · US

Funding

FGF23 and Cardiovascular Disease in CKDR01DK081374 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WOLF, MYLES S · 2008 to 2016
$4.2M
Role of FGF-23 in Mineral Metabolism Across the Spectum of Chronic Kidney DiseaseR01DK076116 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WOLF, MYLES S · 2007 to 2016
$2.9M
NIDDK NIH HHS R01 DK076116NIDDK NIH HHS R01DK076116NIDDK NIH HHS R01 DK081374NIDDK NIH HHS R01DK081374
6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a public health epidemic that affects millions of people worldwide. Presence of CKD predisposes individuals to high risks of end-stage renal disease (ESRD), cardiovascular disease, and premature death. Disordered phosphate homeostasis with elevated circulating levels of fibroblast growth factor 23 (FGF23) is an early and pervasive complication of CKD. CKD is likely the most common cause of chronically elevated FGF23 levels, and the clinical condition in which levels are most markedly elevated. Although increases in FGF23 levels help maintain serum phosphate in the normal range in CKD, prospective studies in populations of pre-dialysis CKD, incident and prevalent ESRD, and kidney transplant recipients demonstrate that elevated FGF23 levels are independently associated with progression of CKD and development of cardiovascular events and mortality. It was originally thought that these observations were driven by elevated FGF23 levels acting as a highly sensitive biomarker of toxicity due to phosphate. However, FGF23 itself has now been shown to mediate 'off-target,' direct, end-organ toxicity in the heart, which suggests that elevated FGF23 levels may be a novel mechanism of adverse outcomes in CKD. This report reviews recent advances in FGF23 biology relevant to CKD, the classical effects of FGF23 on mineral homeostasis, and the studies that established FGF23 excess as a biomarker and novel mechanism of cardiovascular disease. The report concludes with a critical review of the effects of different therapeutic strategies targeting FGF23 reduction and how these might be leveraged in a future randomized trial aimed at improving outcomes in CKD.

Indexed as

BiomarkersCardiovascular DiseasesDisease ProgressionFibroblast Growth Factor-23Fibroblast Growth FactorsHomeostasisHumansKidneyKidney Failure, ChronicPhosphatesRenal Insufficiency, ChronicUp-RegulationBiomarkersFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsPhosphates

Identifiers

PMID22622492
PMCPMC3434320
OpenAlexW1983098935

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.