Evidence map›Paper›PMID 29167171›Full record

ReviewAmerican journal of physiology. Renal physiology2018

Advances in our understanding of the pathogenesis of hemolytic uremic syndromes.

E E Bowen, R J Coward

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Escherichia coli O157:H7 strains in bovine carcasses and the impact on the animal production chain.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Complement in Secondary Thrombotic Microangiopathy.Kidney international reports · 2021
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. 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

2 authors at 1 institution in 1 country.

E E BowenAcademic Renal Unit, School of Clinical Sciences, University of Bristol , Bristol , United Kingdom.
R J CowardAcademic Renal Unit, School of Clinical Sciences, University of Bristol , Bristol , United Kingdom.
University of Bristol · GB

Funding

Medical Research Council MR/K010492/1
6 · The paper itself

Abstract

Hemolytic uremic syndrome (HUS) is major global health care issue as it is the leading cause of acute kidney injury in children. It is a triad of acute kidney injury, microangiopathic hemolytic anemia, and thrombocytopenia. In recent years, major advances in our understanding of complement-driven inherited rare forms of HUS have been achieved. However, in children 90% of cases of HUS are associated with a Shiga toxin-producing enteric pathogen. The precise pathological mechanisms in this setting are yet to be elucidated. The purpose of this review is to discuss advances in our understanding of the pathophysiology underlying HUS and identify the key questions yet to be answered by the scientific community.

Indexed as

Complement ActivationAcute Kidney InjuryAnimalsAtypical Hemolytic Uremic SyndromeComplement System ProteinsEscherichia coli InfectionsGenetic Predisposition to DiseaseHumansPhenotypePrognosisRisk FactorsShiga-Toxigenic Escherichia coliThrombotic MicroangiopathiesComplement System Proteinscomplementhemolytic uremic syndromethrombotic microangiopathy

Identifiers

PMID29167171
PMCPMC5899223
OpenAlexW2770603183

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.