Evidence mapPaperPMID 32260373Full record

ReviewToxins2020

Inflammation and Premature Ageing in Chronic Kidney Disease.

Thomas Ebert, Sven-Christian Pawelzik, Anna Witasp, Samsul Arefin, Sam Hobson, Karolina Kublickiene, Paul G Shiels, Magnus Bäck, Peter Stenvinkel

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 2 pooled it
17.2field-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

142 citing papers in PubMed, 2 syntheses or guidelines pooled it, 226 citations in OpenAlex.

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82 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

9 authors at 3 institutions in 2 countries.

Thomas EbertKarolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden.ORCID 0000-0003-1683-9276
Sven-Christian PawelzikKarolinska Institutet, Department of Medicine Solna, Cardiovascular Medicine Unit, SE-171 76 Stockholm, Sweden.
Anna WitaspKarolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden.
Samsul ArefinKarolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden.
Sam HobsonKarolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden.
Karolina KublickieneKarolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden.
Paul G ShielsUniversity of Glasgow, Wolfson Wohl Cancer Research Centre, College of Medical, Veterinary & Life Sciences, Institute of Cancer Sciences, Glasgow G61 1QH, UK.
Magnus BäckKarolinska Institutet, Department of Medicine Solna, Cardiovascular Medicine Unit, SE-171 76 Stockholm, Sweden.ORCID 0000-0003-0853-5141
Peter StenvinkelKarolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden.
Karolinska Institutet · SEKarolinska University Hospital · SEUniversity of Glasgow · GB

Funding

King Gustaf V and Queen Victoria Freemason Foundation N/ANjurfonden (Swedish Kidney Foundation)Novo Nordisk Novo Nordisk postdoctoral fellowship run in partnership with Karolinska Institutet, Stockholm, SwedenProfessor Nanna Svartz Foundation N/AStockholms Läns Landsting 20170365Swedish Heart and Lung Foundation 20180571 and 20160384Vetenskapsrådet 2009-1068Vetenskapsrådet 2018-00932
6 · The paper itself

Abstract

Persistent low-grade inflammation and premature ageing are hallmarks of the uremic phenotype and contribute to impaired health status, reduced quality of life, and premature mortality in chronic kidney disease (CKD). Because there is a huge global burden of disease due to CKD, treatment strategies targeting inflammation and premature ageing in CKD are of particular interest. Several distinct features of the uremic phenotype may represent potential treatment options to attenuate the risk of progression and poor outcome in CKD. The nuclear factor erythroid 2-related factor 2 (NRF2)-kelch-like erythroid cell-derived protein with CNC homology [ECH]-associated protein 1 (KEAP1) signaling pathway, the endocrine phosphate-fibroblast growth factor-23-klotho axis, increased cellular senescence, and impaired mitochondrial biogenesis are currently the most promising candidates, and different pharmaceutical compounds are already under evaluation. If studies in humans show beneficial effects, carefully phenotyped patients with CKD can benefit from them.

Indexed as

Aging, PrematureAnimalsBiomarkersHealth StatusHumansInflammationInflammation MediatorsKidneyPhenotypePrognosisQuality of LifeRenal Insufficiency, ChronicRisk FactorsSignal TransductionToxins, BiologicalUremiaBiomarkersInflammation MediatorsToxins, Biologicalageingchronic kidney diseaseend-stage kidney diseaseinflammationpremature ageingsenescenceuremic toxins

Identifiers

PMID32260373
PMCPMC7232447
OpenAlexW3015068556

What Socratic holds

Textmetadata
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 Socratic graph.