Evidence map›Paper›PMID 40102634›Full record

ReviewNature reviews. Nephrology2025

Neutrophils and NETs in kidney disease.

Daigo Nakazawa, Sakiko Masuda, Yuka Nishibata, Kanako Watanabe-Kusunoki, Utano Tomaru, Akihiro Ishizu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–field-weighted citation impact
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

34 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Microbiota-gut-kidney axis in health and renal disease.International journal of biological sciences · 2026
    Review
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

6 authors.

Daigo NakazawaDepartment of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.ORCID http://orcid.org/0000-0003-3735-4630
Sakiko MasudaDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
Yuka NishibataDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.ORCID http://orcid.org/0009-0002-6971-0652
Kanako Watanabe-KusunokiDepartment of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Utano TomaruDepartment of Surgical Pathology, Hokkaido University Hospital, Sapporo, Japan.
Akihiro IshizuDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan. aishizu@med.hokudai.ac.jp.ORCID http://orcid.org/0000-0002-7084-9734

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils, conventionally regarded as a homogeneous immune cell population, have emerged as a heterogeneous group of cells with distinct gene profiles and immune properties. Activated neutrophils release a spectrum of bioactive substances, including cytokines, chemokines, proteolytic enzymes, reactive oxygen species and neutrophil extracellular traps (NETs), which are composed of decondensed DNA and antimicrobial proteins. NETs have a pivotal role in innate immunity, including in preventing the ascent of uropathogenic bacteria into the kidneys, as they efficiently trap pathogenic microorganisms. However, although indispensable for defence against pathogens, NETs also pose risks of self-damage owing to their cytotoxicity, thrombogenicity and autoantigenicity. Accordingly, neutrophils and NETs have been implicated in the pathogenesis of various disorders that affect the kidneys, including acute kidney injury, vasculitis, systemic lupus erythematosus, thrombotic microangiopathy and in various aetiologies of chronic kidney disease. Pathological alterations in the glomerular vascular wall can promote the infiltration of neutrophils, which can cause tissue damage and inflammation through their interactions with kidney-resident cells, including mesangial cells and podocytes, leading to local cell death. Targeting neutrophil activation and NET formation might therefore represent a new therapeutic strategy for these conditions.

Indexed as

Extracellular TrapsKidney DiseasesNeutrophilsAnimalsHumansImmunity, Innate

Identifiers

PMID40102634

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.