Evidence map›Paper›PMID 37775316›Full record

ArticleNeurology2023

Interplay Between Chronic Kidney Disease, Hypertension, and Stroke: Insights From a Multivariable Mendelian Randomization Analysis.

Dearbhla M Kelly, Marios K Georgakis, Nora Franceschini, Deborah Blacker, Anand Viswanathan, Christopher D Anderson

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
14.1field-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

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

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  19. The predictive valueFrontiers in medicine · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 2 countries.

Dearbhla M KellyFrom the J. Philip Kistler Stroke Research Center (D.M.K., A.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School; Program in Medical and Population Genetics (D.M.K., M.K.G., C.D.A.), Broad Institute of Harvard and the Massachusetts Institute of Technology, Boston; Institute for Stroke and Dementia Research (M.K.G.), University Hospital of LMU Munich, Germany; McCance Center for Brain Health (M.K.G., C.D.A.), Massachusetts General Hospital, Boston; Department of Epidemiology (N.F.), University of North Carolina, Chapel Hill; Department of Psychiatry (D.B.), Massachusetts General Hospital, Harvard Medical School; Department of Epidemiology (D.B.), Harvard T.H. Chan School of Public Health; and Department of Neurology (C.D.A.), Brigham and Women's Hospital, Boston, MA. dearbhlakelly2@gmail.com.ORCID https://orcid.org/0000-0002-4318-2030
Marios K GeorgakisFrom the J. Philip Kistler Stroke Research Center (D.M.K., A.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School; Program in Medical and Population Genetics (D.M.K., M.K.G., C.D.A.), Broad Institute of Harvard and the Massachusetts Institute of Technology, Boston; Institute for Stroke and Dementia Research (M.K.G.), University Hospital of LMU Munich, Germany; McCance Center for Brain Health (M.K.G., C.D.A.), Massachusetts General Hospital, Boston; Department of Epidemiology (N.F.), University of North Carolina, Chapel Hill; Department of Psychiatry (D.B.), Massachusetts General Hospital, Harvard Medical School; Department of Epidemiology (D.B.), Harvard T.H. Chan School of Public Health; and Department of Neurology (C.D.A.), Brigham and Women's Hospital, Boston, MA.
Nora FranceschiniFrom the J. Philip Kistler Stroke Research Center (D.M.K., A.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School; Program in Medical and Population Genetics (D.M.K., M.K.G., C.D.A.), Broad Institute of Harvard and the Massachusetts Institute of Technology, Boston; Institute for Stroke and Dementia Research (M.K.G.), University Hospital of LMU Munich, Germany; McCance Center for Brain Health (M.K.G., C.D.A.), Massachusetts General Hospital, Boston; Department of Epidemiology (N.F.), University of North Carolina, Chapel Hill; Department of Psychiatry (D.B.), Massachusetts General Hospital, Harvard Medical School; Department of Epidemiology (D.B.), Harvard T.H. Chan School of Public Health; and Department of Neurology (C.D.A.), Brigham and Women's Hospital, Boston, MA.ORCID https://orcid.org/0009-0001-8346-3662
Deborah BlackerFrom the J. Philip Kistler Stroke Research Center (D.M.K., A.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School; Program in Medical and Population Genetics (D.M.K., M.K.G., C.D.A.), Broad Institute of Harvard and the Massachusetts Institute of Technology, Boston; Institute for Stroke and Dementia Research (M.K.G.), University Hospital of LMU Munich, Germany; McCance Center for Brain Health (M.K.G., C.D.A.), Massachusetts General Hospital, Boston; Department of Epidemiology (N.F.), University of North Carolina, Chapel Hill; Department of Psychiatry (D.B.), Massachusetts General Hospital, Harvard Medical School; Department of Epidemiology (D.B.), Harvard T.H. Chan School of Public Health; and Department of Neurology (C.D.A.), Brigham and Women's Hospital, Boston, MA.
Anand ViswanathanFrom the J. Philip Kistler Stroke Research Center (D.M.K., A.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School; Program in Medical and Population Genetics (D.M.K., M.K.G., C.D.A.), Broad Institute of Harvard and the Massachusetts Institute of Technology, Boston; Institute for Stroke and Dementia Research (M.K.G.), University Hospital of LMU Munich, Germany; McCance Center for Brain Health (M.K.G., C.D.A.), Massachusetts General Hospital, Boston; Department of Epidemiology (N.F.), University of North Carolina, Chapel Hill; Department of Psychiatry (D.B.), Massachusetts General Hospital, Harvard Medical School; Department of Epidemiology (D.B.), Harvard T.H. Chan School of Public Health; and Department of Neurology (C.D.A.), Brigham and Women's Hospital, Boston, MA.
Christopher D AndersonFrom the J. Philip Kistler Stroke Research Center (D.M.K., A.V.), Department of Neurology, Massachusetts General Hospital, Harvard Medical School; Program in Medical and Population Genetics (D.M.K., M.K.G., C.D.A.), Broad Institute of Harvard and the Massachusetts Institute of Technology, Boston; Institute for Stroke and Dementia Research (M.K.G.), University Hospital of LMU Munich, Germany; McCance Center for Brain Health (M.K.G., C.D.A.), Massachusetts General Hospital, Boston; Department of Epidemiology (N.F.), University of North Carolina, Chapel Hill; Department of Psychiatry (D.B.), Massachusetts General Hospital, Harvard Medical School; Department of Epidemiology (D.B.), Harvard T.H. Chan School of Public Health; and Department of Neurology (C.D.A.), Brigham and Women's Hospital, Boston, MA.
Broad Institute · US

Funding

THE ROLE OF ADVANCED CAA IN ALZHEIMER'S DEMENTIAP50AG005134 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1985 to 2018
$42.1M
Validation of Small-Vessel Disease Neuroimaging Biomarkers in Cerebral Amyloid Angiopathy-Related Cognitive DeclineR01NS104130 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI VISWANATHAN, ANAND · 2018 to 2022
$3.4M
Sequencing Annotation and Functional Analysis in Risk of Intracerebral HemorrhageR01NS103924 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ANDERSON, CHRISTOPHER DAVID · 2018 to 2022
$3.4M
Genetics of Cardiovascular Disease in Chronic Kidney DiseaseR01HL163972 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FRANCESCHINI, NORA, LI, YUN · 2022 to 2025
$1.9M
NHLBI NIH HHS R01 HL163972NIA NIH HHS P50 AG005134NINDS NIH HHS R01 NS103924NINDS NIH HHS R01 NS104130
6 · The paper itself

Abstract

BACKGROUND AND

objectivesChronic kidney disease (CKD) increases the risk of stroke, but the extent through which this association is mediated by hypertension is unknown. We leveraged large-scale genetic data to explore causal relationships between CKD, hypertension, and cerebrovascular disease phenotypes.

methodsWe used data from genome-wide association studies of European ancestry to identify genetic proxies for kidney function (CKD diagnosis, estimated glomerular filtration rate [eGFR], and urinary albumin-to-creatinine ratio [UACR]), systolic blood pressure (SBP), and cerebrovascular disease (ischemic stroke and its subtypes and intracerebral hemorrhage). We then conducted univariable, multivariable, and mediation Mendelian randomization (MR) analyses to investigate the effect of kidney function on stroke risk and the proportion of this effect mediated through hypertension.

resultsUnivariable MR revealed associations between genetically determined lower eGFR and risk of all stroke (odds ratio [OR] per 1-log decrement in eGFR, 1.77; 95% CI 1.31-2.40; DISCUSSION: Our results demonstrate an independent causal effect of impaired kidney function, as assessed by decreased eGFR, on stroke risk, particularly LAS, even when controlled for SBP. Targeted prevention of kidney disease could lower atherosclerotic stroke risk independent of hypertension.

Indexed as

Cerebrovascular DisordersHypertensionIschemic StrokeRenal Insufficiency, ChronicStrokeGenome-Wide Association StudyHumansMendelian Randomization Analysis

Identifiers

PMID37775316
PMCPMC10662984
OpenAlexW4387161470

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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.