Evidence map›Paper›PMID 29698460›Full record

Observational studyPloS one2018

Growth differentiation factor-15 and fibroblast growth factor-23 are associated with mortality in type 2 diabetes - An observational follow-up study.

Marie Frimodt-Møller, Bernt Johan von Scholten, Henrik Reinhard, Peter Karl Jacobsen, Tine Willum Hansen, Frederik Ivar Persson, Hans-Henrik Parving, Peter Rossing

Open access · goldAbstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Marie Frimodt-MøllerSteno Diabetes Center Copenhagen, Copenhagen, Denmark.ORCID 0000-0002-8486-1515
Bernt Johan von ScholtenSteno Diabetes Center Copenhagen, Copenhagen, Denmark.
Henrik ReinhardSteno Diabetes Center Copenhagen, Copenhagen, Denmark.
Peter Karl JacobsenDepartment of Cardiology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.
Tine Willum HansenSteno Diabetes Center Copenhagen, Copenhagen, Denmark.
Frederik Ivar PerssonSteno Diabetes Center Copenhagen, Copenhagen, Denmark.
Hans-Henrik ParvingDepartment of Medical Endocrinology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.
Peter RossingSteno Diabetes Center Copenhagen, Copenhagen, Denmark.
Steno Diabetes Centers · DKUniversity of Copenhagen · DKCopenhagen University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTwo biomarkers, growth differentiation factor 15 (GDF-15) and fibroblast growth factor 23 (FGF-23)), reflecting different aspects of renal pathophysiology, were evaluated as determinants of decline in estimated glomerular filtration rate (eGFR), incident cardiovascular disease (CVD) and all-cause mortality in patients with type 2 diabetes (T2D) and microalbuminuria, but without clinical cardiac disease. MATERIALS AND

methodsProspective study including 200 T2D patients. The predefined endpoint of chronic kidney disease (CKD) progression: A decline in eGFR of >30% at any time point during follow-up. Hazard ratios (HR) are provided per 1 SD increment of log2-transformed values.

resultsMean (± SD) age was 59 ± 9 years, eGFR 91.1 ± 18.3 ml/min/1.73m2 and median (IQR) UAER 103 (39-230) mg/24-h. During a median 6.1 years follow-up, 40 incident CVD events, 26 deaths and 42 patients reached the CKD endpoint after median 4.9 years. Higher GDF-15 was a determinant of decline in eGFR >30% and all-cause mortality in adjusted models (HR 1.7 (1.1-2.5); p = 0.018 and HR 1.9 (1.2-2.9); p = 0.003, respectively). Adding GDF-15 to traditional risk factors improved risk prediction of decline in renal function (relative integrated discrimination improvement (rIDI) = 30%; p = 0.037). Higher FGF-23 was associated with all-cause mortality in adjusted models (HR 1.6 (1.1-2.2); p = 0.011) with a rIDI of 30% (p = 0.024).

conclusionsIn patients with T2D and microalbuminuria, higher GDF-15 and FGF-23 were independently associated with all-cause mortality and higher GDF-15 improved risk prediction of decline in kidney function and higher FGF-23 of all-cause mortality, beyond traditional risk factors, but not independently of GDF-15.

Indexed as

AgedAlbuminuriaCardiovascular DiseasesCause of DeathDiabetes Mellitus, Type 2FemaleFibroblast Growth Factor-23Fibroblast Growth FactorsFollow-Up StudiesGlomerular Filtration RateGrowth Differentiation Factor 15HumansIncidenceKaplan-Meier EstimateMaleMiddle AgedFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsGDF15 protein, humanGrowth Differentiation Factor 15

Identifiers

PMID29698460
PMCPMC5919646
OpenAlexW2799677404

What OpenQuestion holds

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LicenceCC BY
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.