Evidence map›Paper›PMID 27609359›Full record

SynthesisBMC nephrology2016

Effect of mineralocorticoid receptor antagonists on proteinuria and progression of chronic kidney disease: a systematic review and meta-analysis.

Gemma Currie, Alison H M Taylor, Toshiro Fujita, Hiroshi Ohtsu, Morten Lindhardt, Peter Rossing, Lene Boesby, Nicola C Edwards, Charles J Ferro, Jonathan N Townend and 7 more

Open access · goldAbstract readMeta-AnalysisSystematic Review
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in BMC nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 7 pooled it
10.2field-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

94 citing papers in PubMed, 7 syntheses or guidelines pooled it, 204 citations in OpenAlex.

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  19. The Synergistic Treatment of Heart and Kidney Disease.Deutsches Arzteblatt international · 2026
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34 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

17 authors at 10 institutions in 6 countries.

Gemma CurrieInstitute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Center, 126 University Place, Glasgow, UK. gemma.currie@glasgow.ac.uk.ORCID 0000-0002-0797-0224
Alison H M TaylorInstitute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Center, 126 University Place, Glasgow, UK.
Toshiro FujitaDivision of Clinical Epigenetics, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.
Hiroshi OhtsuDepartment of Clinical Study and Informatics, Center for Clinical Sciences, National Center for Global Health and Medicine, Tokyo, Japan.
Morten LindhardtSteno Diabetes Center, Niels Steensens Vej, Gentofte, Denmark.
Peter RossingSteno Diabetes Center, Niels Steensens Vej, Gentofte, Denmark.
Lene BoesbyDepartment of Nephrology, Herlev Hospital, University of Copenhagen, Herlev, Denmark.
Nicola C EdwardsDepartments of Cardiology and Nephrology, University Hospital Birmingham and School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, UK.
Charles J FerroDepartments of Cardiology and Nephrology, University Hospital Birmingham and School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, UK.
Jonathan N TownendDepartments of Cardiology and Nephrology, University Hospital Birmingham and School of Clinical and Experimental Medicine, University of Birmingham, Birmingham, UK.
Anton H van den MeirackerDepartment of Internal Medicine and Pharmacy, Erasmus MC, Rotterdam, The Netherlands.
Mohammad G SaklayenVA Medical Center, 4100 West Third St, Dayton, OH, 45428, USA.
Sonia OveisiMetabolic Diseases Research Center, Qazvin University of Medical Sciences, Qazvin, Iran.
Alan G JardineInstitute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Center, 126 University Place, Glasgow, UK.
Christian DellesInstitute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Center, 126 University Place, Glasgow, UK.
David J PreissClinical Trial Service Unit and Epidemiological Studies Unit, University of Oxford, Oxford, UK.
Patrick B MarkInstitute of Cardiovascular and Medical Sciences, British Heart Foundation Glasgow Cardiovascular Research Center, 126 University Place, Glasgow, UK.
British Heart Foundation · GBNIHR Surgical Reconstruction and Microbiology Research Centre · GBUniversity of Copenhagen · DKDayton VA Medical Center · USErasmus MC · NLNational Center for Global Health and Medicine · JPQazvin University of Medical Sciences · IRSteno Diabetes Centers · DKThe University of Tokyo · JPUniversity of Oxford · GB

Funding

British Heart Foundation SP/12/8/29620
6 · The paper itself

Abstract

backgroundHypertension and proteinuria are critically involved in the progression of chronic kidney disease. Despite treatment with renin angiotensin system inhibition, kidney function declines in many patients. Aldosterone excess is a risk factor for progression of kidney disease. Hyperkalaemia is a concern with the use of mineralocorticoid receptor antagonists. We aimed to determine whether the renal protective benefits of mineralocorticoid antagonists outweigh the risk of hyperkalaemia associated with this treatment in patients with chronic kidney disease.

methodsWe conducted a meta-analysis investigating renoprotective effects and risk of hyperkalaemia in trials of mineralocorticoid receptor antagonists in chronic kidney disease. Trials were identified from MEDLINE (1966-2014), EMBASE (1947-2014) and the Cochrane Clinical Trials Database. Unpublished summary data were obtained from investigators. We included randomised controlled trials, and the first period of randomised cross over trials lasting ≥4 weeks in adults.

resultsNineteen trials (21 study groups, 1 646 patients) were included. In random effects meta-analysis, addition of mineralocorticoid receptor antagonists to renin angiotensin system inhibition resulted in a reduction from baseline in systolic blood pressure (-5.7 [-9.0, -2.3] mmHg), diastolic blood pressure (-1.7 [-3.4, -0.1] mmHg) and glomerular filtration rate (-3.2 [-5.4, -1.0] mL/min/1.73 m(2)). Mineralocorticoid receptor antagonism reduced weighted mean protein/albumin excretion by 38.7 % but with a threefold higher relative risk of withdrawing from the trial due to hyperkalaemia (3.21, [1.19, 8.71]). Death, cardiovascular events and hard renal end points were not reported in sufficient numbers to analyse.

conclusionsMineralocorticoid receptor antagonism reduces blood pressure and urinary protein/albumin excretion with a quantifiable risk of hyperkalaemia above predefined study upper limit.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsBlood PressureDisease ProgressionGlomerular Filtration RateHumansHyperkalemiaMineralocorticoid Receptor AntagonistsPatient DropoutsProteinuriaRandomized Controlled Trials as TopicRenal Insufficiency, ChronicRisk AssessmentAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsMineralocorticoid Receptor Antagonists

Identifiers

PMID27609359
PMCPMC5015203
OpenAlexW2510521632

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.