Evidence map›Paper›PMID 27188921›Full record

ReviewNature reviews. Disease primers2015

Diabetic kidney disease.

Merlin C Thomas, Michael Brownlee, Katalin Susztak, Kumar Sharma, Karin A M Jandeleit-Dahm, Sophia Zoungas, Peter Rossing, Per-Henrik Groop, Mark E Cooper

Open access · bronzeAbstract readReview
In one paragraph

Review in Nature reviews. Disease primers, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 784 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
784citing papers in PubMed, 6 pooled it
9.0field-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

784 citing papers in PubMed, 6 syntheses or guidelines pooled it, 1,166 citations in OpenAlex.

  1. The Role ofGenes · 2026
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  6. The Role ofGenes · 2025
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  16. Total flavonoids ofPharmaceutical biology · 2026
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724 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 7 institutions in 4 countries.

Merlin C ThomasBaker IDI Heart &Diabetes Institute, 75 Commercial Road, Melbourne, Victoria 3004, Australia.
Michael BrownleeAlbert Einstein College of Medicine, Bronx, New York, New York, USA.
Katalin SusztakPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Kumar SharmaCenter for Renal Translational Medicine, University of California, San Diego, California, USA.
Karin A M Jandeleit-DahmBaker IDI Heart &Diabetes Institute, 75 Commercial Road, Melbourne, Victoria 3004, Australia.
Sophia ZoungasDepartment of Epidemiology and Preventative Medicine, Faculty of Medicine, Nursing &Health Sciences, Monash University, Melbourne, Victoria, Australia.
Peter RossingSteno Diabetes Center, Gentofte, Denmark.
Per-Henrik GroopDepartment of Nephrology, University of Helsinki, Helsinki, Finland.
Mark E CooperBaker IDI Heart &Diabetes Institute, 75 Commercial Road, Melbourne, Victoria 3004, Australia.
Baker Heart and Diabetes Institute · AUAlbert Einstein College of Medicine · USMonash University · AUSteno Diabetes Center · DKUniversity of California, San Diego · USUniversity of Helsinki · FIUniversity of Pennsylvania · US

Funding

Role of the Notch Pathway in Kidney InjuryR01DK076077 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2007 to 2026
$8.0M
Epigenetics of Chronic Kidney DiseaseR01DK087635 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2009 to 2026
$7.0M
APOL1 associated kidney diseaseR01DK105821 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SUSZTAK, KATALIN · 2016 to 2024
$4.6M
Epigenetic drivers and biomarkers of diabetic kidney diseaseDP3DK108220 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SUSZTAK, KATALIN · 2015 to 2015
$2.4M
NIDDK NIH HHS DP3 DK108220NIDDK NIH HHS R01 DK076077NIDDK NIH HHS R01 DK087635NIDDK NIH HHS R01 DK105821
6 · The paper itself

Abstract

The kidney is arguably the most important target of microvascular damage in diabetes. A substantial proportion of individuals with diabetes will develop kidney disease owing to their disease and/or other co-morbidity, including hypertension and ageing-related nephron loss. The presence and severity of chronic kidney disease (CKD) identify individuals who are at increased risk of adverse health outcomes and premature mortality. Consequently, preventing and managing CKD in patients with diabetes is now a key aim of their overall management. Intensive management of patients with diabetes includes controlling blood glucose levels and blood pressure as well as blockade of the renin-angiotensin-aldosterone system; these approaches will reduce the incidence of diabetic kidney disease and slow its progression. Indeed, the major decline in the incidence of diabetic kidney disease (DKD) over the past 30 years and improved patient prognosis are largely attributable to improved diabetes care. However, there remains an unmet need for innovative treatment strategies to prevent, arrest, treat and reverse DKD. In this Primer, we summarize what is now known about the molecular pathogenesis of CKD in patients with diabetes and the key pathways and targets implicated in its progression. In addition, we discuss the current evidence for the prevention and management of DKD as well as the many controversies. Finally, we explore the opportunities to develop new interventions through urgently needed investment in dedicated and focused research. For an illustrated summary of this Primer, visit: http://go.nature.com/NKHDzg.

Indexed as

Blood GlucoseBlood PressureDiabetes MellitusDiabetic NephropathiesDisease ManagementDisease ProgressionHumansHypertensionKidneyRenal Insufficiency, ChronicRenin-Angiotensin SystemBlood Glucose

Identifiers

PMID27188921
PMCPMC7724636
OpenAlexW2394782024

What Socratic holds

Textmetadata
LicenceTDM
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.