Evidence map›Paper›PMID 26079688›Full record

Trial reportPloS one2015

Relation between Red Cell Distribution Width and Fibroblast Growth Factor 23 Cleaving in Patients with Chronic Kidney Disease and Heart Failure.

Fenna van Breda, Mireille E Emans, Karien van der Putten, Branko Braam, Frans J van Ittersum, Rob J Kraaijenhagen, Martin H de Borst, Marc Vervloet, Carlo A J M Gaillard

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.3field-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

7 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Acute blood loss stimulates fibroblast growth factor 23 production.American journal of physiology. Renal physiology · 2018
    Article
  5. Article
  6. Predictive Values of Red Blood Cell Distribution Width in Assessing Severity of Chronic Heart Failure.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  7. 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

9 authors at 6 institutions in 2 countries.

Fenna van BredaDepartment of Nephrology and ICaR-VU, VUMC, Amsterdam, the Netherlands.
Mireille E EmansDepartment of Cardiology, Ikazia Hospital, Rotterdam, the Netherlands.
Karien van der PuttenDepartment of Internal Medicine, TerGooi Hospital, Hilversum, the Netherlands.
Branko BraamDepartment of Medicine, division of Nephrology and Immunology, University of Alberta, Edmonton, Canada.
Frans J van IttersumDepartment of Nephrology and ICaR-VU, VUMC, Amsterdam, the Netherlands.
Rob J KraaijenhagenDepartment of Clinical Chemistry, Meander Medical Center, Amersfoort, the Netherlands.
Martin H de BorstDepartment of Nephrology, UMCG, Groningen, the Netherlands.
Marc VervloetDepartment of Nephrology and ICaR-VU, VUMC, Amsterdam, the Netherlands.
Carlo A J M GaillardDepartment of Nephrology, UMCG, Groningen, the Netherlands.
Amsterdam UMC Location VUmc · NLDialyse Centrum Groningen · NLIkazia Ziekenhuis · NLMeander Medisch Centrum · NLTergooi · NLUniversity of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIn chronic kidney disease (CKD), both anemia and deregulated phosphate metabolism are common and predictive of adverse outcome. Previous studies suggest that iron status influences phosphate metabolism by modulating proteolytic cleavage of FGF23 into C-terminal fragments. Red cell distribution width (RDW) was recently identified as a strong prognostic determinant for cardiovascular morbidity and mortality, independently of iron status. We assessed whether RDW is associated with FGF23 cleaving in CKD patients with heart failure. MATERIALS AND

methodsThe associations between RDW and either intact FGF23 (iFGF23), C-terminal FGF23 (cFGF23, reflecting iFGF23 and C-terminal fragments together) and the iFGF23/cFGF23 ratio were analyzed in 52 patients with CKD (eGFR 34,9 ± 13.9 ml/min/1.73m2) and chronic heart failure (CHF). Associations between RDW and FGF23 forms were studied by linear regression analysis adjusted for parameters of renal function, iron metabolism, phosphate metabolism and inflammation.

resultsMedian cFGF23 levels were 197.5 [110-408.5] RU/ml, median iFGF23 levels were 107.3 [65.1-162.2] pg/ml and median FGF23 ratio was 0.80 [0.37-0.86]. Mean RDW was 14.1 ± 1.2%. cFGF23 and RDW were associated (β = 1.63 x 10(-3), P < 0.001), whereas iFGF23 and RDW were not (β = -1.38 x 10(-3), P = 0.336). The iFGF23/cFGF23 ratio was inversely associated with RDW. The difference between cFGF23 and iFGF23 (cFGF23- iFGF23) was positively associated with RDW (β = 1.74 x 10(-3), P < 0.001). The association between cFGF23 and RDW persisted upon multivariable linear regression analysis, adjusted for parameters of renal function, phosphate metabolism, iron metabolism and inflammation (β = 0.97 x 10(-3), P = 0.047).

conclusionRDW is associated with cFGF23 but not with iFGF23 levels in patients with CKD and CHF. This suggests a connection between RDW and FGF23 catabolism, independent of iron status and inflammation. Future studies are needed to unravel underlying mechanisms and whether these pertain to the link between RDW and outcome.

Indexed as

AgedAged, 80 and overCross-Sectional StudiesErythrocyte IndicesFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsHeart FailureHumansMaleMultivariate AnalysisRenal Insufficiency, ChronicFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth Factors

Identifiers

PMID26079688
PMCPMC4469605
OpenAlexW2136302759

What OpenQuestion holds

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LicenceCC BY
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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.