Evidence map›Paper›PMID 36930632›Full record

ArticlePloS one2023

Marker for kidney fibrosis is associated with inflammation and deterioration of kidney function in people with type 2 diabetes and microalbuminuria.

Christina Gjerlev Poulsen, Daniel G K Rasmussen, Federica Genovese, Tine W Hansen, Signe Holm Nielsen, Henrik Reinhard, Bernt Johan von Scholten, Peter K Jacobsen, Hans-Henrik Parving, Morten Asser Karsdal and 2 more

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In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 14 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

12 authors at 3 institutions in 1 country.

Christina Gjerlev PoulsenSteno Diabetes Center Copenhagen, Herlev, Denmark.ORCID 0000-0002-4355-3081
Daniel G K RasmussenNordic Bioscience, Herlev, Denmark.
Federica GenoveseNordic Bioscience, Herlev, Denmark.
Tine W HansenSteno Diabetes Center Copenhagen, Herlev, Denmark.
Signe Holm NielsenNordic Bioscience, Herlev, Denmark.
Henrik ReinhardSteno Diabetes Center Copenhagen, Herlev, Denmark.
Bernt Johan von ScholtenSteno Diabetes Center Copenhagen, Herlev, Denmark.
Peter K JacobsenDepartment of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Hans-Henrik ParvingDepartment of Endocrinology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Morten Asser KarsdalNordic Bioscience, Herlev, Denmark.
Peter RossingSteno Diabetes Center Copenhagen, Herlev, Denmark.ORCID 0000-0002-1531-4294
Marie Frimodt-MøllerSteno Diabetes Center Copenhagen, Herlev, Denmark.
Steno Diabetes Centers · DKNordic Bioscience (Denmark) · DKUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic kidney disease is a major cause of morbidity and mortality. Dysregulated turnover of collagen type III is associated with development of kidney fibrosis. We investigated whether a degradation product of collagen type III (C3M) was a risk marker for progression of chronic kidney disease (CKD), occurrence of cardiovascular disease (CVD), and mortality during follow up in people with type 2 diabetes (T2D) and microalbuminuria. Moreover, we investigated whether C3M was correlated with markers of inflammation and endothelial dysfunction at baseline.

methodsC3M was measured in serum (sC3M) and urine (uC3M) in 200 participants with T2D and microalbuminuria included in an observational, prospective study at Steno Diabetes Center Copenhagen in Denmark from 2007-2008. Baseline measurements included 12 markers of inflammation and endothelial dysfunction. The endpoints were CVD, mortality, and CKD progression (>30% decline in eGFR).

resultsMean (SD) age was 59 (9) years, eGFR 90 (17) ml/min/1.73m2 and median (IQR) urine albumin excretion rate 102 (39-229) mg/24-h. At baseline all markers for inflammation were positively correlated with sC3M (p≤0.034). Some, but not all, markers for endothelial dysfunction were correlated with C3M. Median follow-up ranged from 4.9 to 6.3 years. Higher sC3M was associated with CKD progression (with mortality as competing risk) with a hazard ratio (per doubling) of 2.98 (95% CI: 1.41-6.26; p = 0.004) adjusted for traditional risk factors. uC3M was not associated with CKD progression. Neither sC3M or uC3M were associated with risk of CVD or mortality.

conclusionsHigher sC3M was a risk factor for chronic kidney disease progression and was correlated with markers of inflammation.

Indexed as

Cardiovascular DiseasesDiabetes Mellitus, Type 2Renal Insufficiency, ChronicBiomarkersCollagen Type IIIDisease ProgressionFibrosisGlomerular Filtration RateHumansInflammationKidneyMiddle AgedProspective StudiesBiomarkersCollagen Type III

Identifiers

PMID36930632
PMCPMC10022760
OpenAlexW4327681267

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LicenceCC BY
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identifiers read8
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Registered trials

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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.