Evidence map›Paper›PMID 30524708›Full record

ReviewClinical kidney journal2018

The potential for improving cardio-renal outcomes by sodium-glucose co-transporter-2 inhibition in people with chronic kidney disease: a rationale for the EMPA-KIDNEY study.

William G Herrington, David Preiss, Richard Haynes, Maximilian von Eynatten, Natalie Staplin, Sibylle J Hauske, Jyothis T George, Jennifer B Green, Martin J Landray, Colin Baigent and 1 more

Erratum issued Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Clinical kidney journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT06890143 (The Efficacy and Safety of Dapagliflozin in the Treatment of Hereditary Kidney Disease With Proteinuria in Children), which is not on this map. Cited by 107 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 5 pooled it
23.1field-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.

NCT06890143 phase3recruitingnot on this mapstarted 2025, after this paper: background citation

The Efficacy and Safety of Dapagliflozin in the Treatment of Hereditary Kidney Disease With Proteinuria in Children: a Prospective, Randomized Crossover Trial

TypeinterventionalSponsorChildren's Hospital of Fudan UniversityRan2025 to 2027Enrolled44ConditionsPediatric Hereditary Kidney DiseasesArmsDapagliflozin+Standard Treatment for 12 weeks,washout period for 4 weeks,then Standard Treatment alone for12 weeks, Standard Treatment alone for 12 weeks ,washout period for 4 weeks ,then Dapagliflozin+Standard Treatment for 12 weeks
3 · Its place in the literature

Who cites it

107 citing papers in PubMed, 5 syntheses or guidelines pooled it, 236 citations in OpenAlex.

  1. Pooled it
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  5. Pooled it
  6. Trial
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  12. Empagliflozin in Patients with Chronic Kidney Disease.The New England journal of medicine · 2023 · on this map
    Trial
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  14. The dapagliflozin and prevention of adverse outcomes in chronic kidney disease (DAPA-CKD) trial: baseline characteristics.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2020
    Trial
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  17. Review
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  19. Treatment Approaches for Alport Syndrome.Journal of the American Society of Nephrology : JASN · 2026
    Review
  20. Article

47 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 3 countries.

William G HerringtonMedical Research Council Population Health Research Unit at the University of Oxford, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
David PreissMedical Research Council Population Health Research Unit at the University of Oxford, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Richard HaynesMedical Research Council Population Health Research Unit at the University of Oxford, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Maximilian von EynattenBoehringer Ingelheim International, Ingelheim, Germany.
Natalie StaplinMedical Research Council Population Health Research Unit at the University of Oxford, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Sibylle J HauskeBoehringer Ingelheim International, Ingelheim, Germany.
Jyothis T GeorgeBoehringer Ingelheim International, Ingelheim, Germany.
Jennifer B GreenDuke Clinical Research Institute, Duke University Medical Center, Durham, NC, USA.
Martin J LandrayMedical Research Council Population Health Research Unit at the University of Oxford, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Colin BaigentMedical Research Council Population Health Research Unit at the University of Oxford, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Christoph WannerWürzburg University Clinic, Würzburg, Germany.
University of Oxford · GBBoehringer Ingelheim (Germany) · DEDuke Medical Center · USMedical Research Council · GB

Funding

Medical Research Council MC_U137686860Medical Research Council MC_UU_12026/4Medical Research Council MR/R007764/1
6 · The paper itself

Abstract

Diabetes is a common cause of chronic kidney disease (CKD), but in aggregate, non-diabetic diseases account for a higher proportion of cases of CKD than diabetes in many parts of the world. Inhibition of the renin-angiotensin system reduces the risk of kidney disease progression and treatments that lower blood pressure (BP) or low-density lipoprotein cholesterol reduce cardiovascular (CV) risk in this population. Nevertheless, despite such interventions, considerable risks for kidney and CV complications remain. Recently, large placebo-controlled outcome trials have shown that sodium-glucose co-transporter-2 (SGLT-2) inhibitors reduce the risk of CV disease (including CV death and hospitalization for heart failure) in people with type 2 diabetes who are at high risk of atherosclerotic disease, and these effects were largely independent of improvements in hyperglycaemia, BP and body weight. In the kidney, increased sodium delivery to the macula densa mediated by SGLT-2 inhibition has the potential to reduce intraglomerular pressure, which may explain why SGLT-2 inhibitors reduce albuminuria and appear to slow kidney function decline in people with diabetes. Importantly, in the trials completed to date, these benefits appeared to be maintained at lower levels of kidney function, despite attenuation of glycosuric effects, and did not appear to be dependent on ambient hyperglycaemia. There is therefore a rationale for studying the cardio-renal effects of SGLT-2 inhibition in people at risk of CV disease and hyperfiltration (i.e. those with substantially reduced nephron mass and/or albuminuria), irrespective of whether they have diabetes.

Indexed as

cardiovascularCKDclinical trialdiabetic kidney diseaseSGLT-2 inhibitor

Identifiers

PMID30524708
PMCPMC6275453
OpenAlexW2898388822

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

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.