Evidence map›Paper›PMID 33219281›Full record

ReviewNature reviews. Nephrology2021

Incretin drugs in diabetic kidney disease: biological mechanisms and clinical evidence.

Radica Z Alicic, Emily J Cox, Joshua J Neumiller, Katherine R Tuttle

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 5 pooled it
12.8field-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

102 citing papers in PubMed, 5 syntheses or guidelines pooled it, 178 citations in OpenAlex.

  1. Pooled it
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  6. Trial
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  13. Cardiorenal outcomes of weight loss interventions in people with CKD and type 2 diabetes.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
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  14. Review
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  20. Kidney and Survival Outcomes with Semaglutide by CKD Severity in the FLOW Trial.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Article

42 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

4 authors at 4 institutions in 1 country.

Radica Z AlicicProvidence Medical Research Center, Providence Health Care, Spokane, WA, USA.ORCID http://orcid.org/0000-0002-5437-5700
Emily J CoxProvidence Medical Research Center, Providence Health Care, Spokane, WA, USA.
Joshua J NeumillerDepartment of Pharmacotherapy, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, USA.
Katherine R TuttleProvidence Medical Research Center, Providence Health Care, Spokane, WA, USA. katherine.tuttle@providence.org.ORCID http://orcid.org/0000-0002-2235-0103
Providence Health & Services · USProvidence Regional Medical Center Everett · USUniversity of Washington · USWashington State University Spokane · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the prevalence of diabetes continues to climb, the number of individuals living with diabetic complications will reach an unprecedented magnitude. The emergence of new glucose-lowering agents - sodium-glucose cotransporter 2 inhibitors and incretin therapies - has markedly changed the treatment landscape of type 2 diabetes mellitus. In addition to effectively lowering glucose, incretin drugs, which include glucagon-like peptide 1 receptor (GLP1R) agonists and dipeptidyl peptidase 4 (DPP4) inhibitors, can also reduce blood pressure, body weight, the risk of developing or worsening chronic kidney disease and/or atherosclerotic cardiovascular events, and the risk of death. Although kidney disease events have thus far been secondary outcomes in clinical trials, an ongoing phase III trial in patients with diabetic kidney disease will test the effect of a GLP1R agonist on a primary kidney disease outcome. Experimental data have identified the modulation of innate immunity and inflammation as plausible biological mechanisms underpinning the kidney-protective effects of incretin-based agents. These drugs block the mechanisms involved in the pathogenesis of kidney damage, including the activation of resident mononuclear phagocytes, tissue infiltration by non-resident inflammatory cells, and the production of pro-inflammatory cytokines and adhesion molecules. GLP1R agonists and DPP4 inhibitors might also attenuate oxidative stress, fibrosis and cellular apoptosis in the kidney.

Indexed as

BiomarkersDiabetes Mellitus, Type 2Diabetic NephropathiesDipeptidyl Peptidase 4Glucagon-Like Peptide 1HumansHypoglycemic AgentsIncretinsKidneyBiomarkersDipeptidyl Peptidase 4DPP4 protein, humanGlucagon-Like Peptide 1Hypoglycemic AgentsIncretins

Identifiers

PMID33219281
OpenAlexW3102119644

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.