Evidence map›Paper›PMID 39567532›Full record

ArticleNature communications2024

Analyzing longitudinal trait trajectories using GWAS identifies genetic variants for kidney function decline.

Simon Wiegrebe, Mathias Gorski, Janina M Herold, Klaus J Stark, Barbara Thorand, Christian Gieger, Carsten A Böger, Johannes Schödel, Florian Hartig, Han Chen and 3 more

Abstract read
In one paragraph

Article in Nature communications, 2024. 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
–field-weighted citation impact
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.

  1. Article
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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

13 authors.

Simon WiegrebeDepartment of Genetic Epidemiology, University of Regensburg, Regensburg, Germany. simon.wiegrebe@stat.uni-muenchen.de.ORCID 0000-0003-3385-6879
Mathias GorskiDepartment of Genetic Epidemiology, University of Regensburg, Regensburg, Germany.ORCID 0000-0002-9103-5860
Janina M HeroldDepartment of Genetic Epidemiology, University of Regensburg, Regensburg, Germany.ORCID 0000-0002-2208-9742
Klaus J StarkDepartment of Genetic Epidemiology, University of Regensburg, Regensburg, Germany.ORCID 0000-0002-7832-1942
Barbara ThorandInstitute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
Christian GiegerInstitute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.ORCID 0000-0001-6986-9554
Carsten A BögerDepartment of Nephrology, University Hospital Regensburg, Regensburg, Germany.
Johannes SchödelDepartment of Nephrology and Hypertension, Uniklinikum Erlangen and Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.ORCID 0000-0002-3587-8839
Florian HartigTheoretical Ecology, University of Regensburg, Regensburg, Germany.
Han ChenHuman Genetics Center, Department of Epidemiology, School of Public Health, The University of Texas Health Science Center at Houston, Houston, TX, USA.ORCID 0000-0002-9510-4923
Thomas W WinklerDepartment of Genetic Epidemiology, University of Regensburg, Regensburg, Germany.ORCID 0000-0003-0292-5421
Helmut KüchenhoffStatistical Consulting Unit StaBLab, Department of Statistics, LMU Munich, Munich, Germany.ORCID 0000-0002-6372-2487
Iris M HeidDepartment of Genetic Epidemiology, University of Regensburg, Regensburg, Germany. iris.heid@klinik.uni-regensburg.de.

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 387509280Deutsche Forschungsgemeinschaft (German Research Foundation) 509149993
6 · The paper itself

Abstract

Understanding the genetics of kidney function decline, or trait change in general, is hampered by scarce longitudinal data for GWAS (longGWAS) and uncertainty about how to analyze such data. We use longitudinal UK Biobank data for creatinine-based estimated glomerular filtration rate from 348,275 individuals to search for genetic variants associated with eGFR-decline. This search was performed both among 595 variants previously associated with eGFR in cross-sectional GWAS and genome-wide. We use seven statistical approaches to analyze the UK Biobank data and simulated data, finding that a linear mixed model is a powerful approach with unbiased effect estimates which is viable for longGWAS. The linear mixed model identifies 13 independent genetic variants associated with eGFR-decline, including 6 novel variants, and links them to age-dependent eGFR-genetics. We demonstrate that age-dependent and age-independent eGFR-genetics exhibit a differential pattern regarding clinical progression traits and kidney-specific gene expression regulation. Overall, our results provide insights into kidney aging and linear mixed model-based longGWAS generally.

Indexed as

Genome-Wide Association StudyGlomerular Filtration RateKidneyAdultAgedAgingCreatinineCross-Sectional StudiesFemaleGenetic VariationHumansLinear ModelsLongitudinal StudiesMaleMiddle AgedPolymorphism, Single NucleotideCreatinine

Identifiers

PMID39567532
PMCPMC11579025

What Socratic holds

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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 Socratic graph.