Evidence map›Paper›PMID 33777361›Full record

ReviewClinical kidney journal2021

The complex interplay between kidney injury and inflammation.

Stephen J McWilliam, Rachael D Wright, Gavin I Welsh, Jack Tuffin, Kelly L Budge, Laura Swan, Thomas Wilm, Ioana-Roxana Martinas, James Littlewood, Louise Oni

Open access · goldAbstract readReview
In one paragraph

Review in Clinical kidney journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Current issues in molecular biology · 2026
    Article
  6. Review
  7. Article
  8. Observational
  9. Review
  10. Article
  11. Review
  12. Renoprotective Potential of Nateglinide in an Acute Kidney Injury Model.International journal of molecular sciences · 2026
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Acute kidney injury and postoperative delirium.Journal of biomedical research · 2025
    Article
  19. Article
  20. Article
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

10 authors at 2 institutions in 1 country.

Stephen J McWilliamDepartment of Paediatric Pharmacology, Alder Hey Children's Hospital, Liverpool, UK.
Rachael D WrightDepartment of Women and Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.ORCID 0000-0002-7606-2297
Gavin I WelshBristol Renal, Bristol Medical School, University of Bristol, Bristol, UK.
Jack TuffinBristol Renal, Bristol Medical School, University of Bristol, Bristol, UK.
Kelly L BudgeDepartment of Women and Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
Laura SwanDepartment of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
Thomas WilmDepartment of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
Ioana-Roxana MartinasDepartment of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
James LittlewoodDepartment of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
Louise OniDepartment of Women and Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.ORCID 0000-0002-1532-2390
University of Liverpool · GBUniversity of Bristol · GB

Funding

Medical Research Council G1000417Medical Research Council MR/N010035/1
6 · The paper itself

Abstract

Acute kidney injury (AKI) has gained significant attention following patient safety alerts about the increased risk of harm to patients, including increased mortality and hospitalization. Common causes of AKI include hypovolaemia, nephrotoxic medications, ischaemia and acute glomerulonephritis, although in reality it may be undetermined or multifactorial. A period of inflammation either as a contributor to the kidney injury or resulting from the injury is almost universally seen. This article was compiled following a workshop exploring the interplay between injury and inflammation. AKI is characterized by some degree of renal cell death through either apoptosis or necrosis, together with a strong inflammatory response. Studies interrogating the resolution of renal inflammation identify a whole range of molecules that are upregulated and confirm that the kidneys are able to intrinsically regenerate after an episode of AKI, provided the threshold of damage is not too high. Kidneys are unable to generate new nephrons, and dysfunctional or repeated episodes will lead to further nephron loss that is ultimately associated with the development of renal fibrosis and chronic kidney disease (CKD). The AKI to CKD transition is a complex process mainly facilitated by maladaptive repair mechanisms. Early biomarkers mapping out this process would allow a personalized approach to identifying patients with AKI who are at high risk of developing fibrosis and subsequent CKD. This review article highlights this process and explains how laboratory models of renal inflammation and injury assist with understanding the underlying disease process and allow interrogation of medications aimed at targeting the mechanistic interplay.

Indexed as

acute kidney injuryglomerulonephritisinflammationrenal fibrosis

Identifiers

PMID33777361
PMCPMC7986351
OpenAlexW3094473528

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.