Evidence map›Paper›PMID 22986362›Full record

ReviewNature reviews. Nephrology2012

Renal and neurological involvement in typical Shiga toxin-associated HUS.

Howard Trachtman, Catherine Austin, Maria Lewinski, Rolf A K Stahl

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 1 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

112 citing papers in PubMed, 1 synthesis or guideline pooled it, 213 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Observational
  5. Review
  6. Article
  7. Article
  8. Nationwide outbreak of Shiga toxin-producingEuro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2026
    Article
  9. Redefining Shiga toxin-induced human cell death as NLRP1- and gasdermin E-mediated pyroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  10. Shiga Toxin Induces ApoptosisJournal of microbiology and biotechnology · 2026
    Article
  11. Article
  12. Shiga Toxin-ProducingKidney international reports · 2025
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Shiga Toxin-Producing E. coli and Hemolytic Uremic Syndrome: A Study of the 2022 Outbreak in Turkey.Medical science monitor : international medical journal of experimental and clinical research · 2024
    Article
  18. Article
  19. Article
  20. Article

52 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 3 institutions in 2 countries.

Howard TrachtmanDepartment of Pediatrics, Division of Nephrology, NYU Langone Medical Center, Clinical Translational Science Institute, Room 712, 227 East 30th Street, New York, NY 10016-9196, USA. Trachtmanhoward.trachtman@nyumc.org
Catherine Austin
Maria Lewinski
Rolf A K Stahl
University Medical Center Hamburg-Eppendorf · DENYU Langone Health · USUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Shiga toxin-producing Escherichia coli-associated haemolytic uraemic syndrome (STEC-HUS) is one of the most important causes of acute kidney injury in patients of all ages, especially in children. It can occur sporadically or in outbreaks. STEC-HUS is a systemic illness caused by toxin-mediated injury to the vascular endothelium and a generalized inflammatory response. The kidney and the brain are the two primary target organs. Nearly 40% of patients with STEC-HUS require at least temporary renal replacement therapy and up to 20% will have permanent residual kidney dysfunction. Neurological injury can be sudden and severe and is the most frequent cause of acute mortality in patients with STEC-HUS. Over the past 30 years, a wide range of inflammatory mediators have been linked to the pathogenesis of STEC-HUS and associated renal and neurological complications. Recently, evidence has accumulated that abnormal activation of the alternative pathway of complement occurs in patients with STEC-HUS. In the large outbreak of STEC-HUS caused by E. coli O104:H4 that occurred in Germany in May 2011, a large number of patients received eculizumab, a monoclonal antibody directed against C5, in an open-label manner. We describe the experience with eculizumab under these emergent circumstances at one large centre.

Indexed as

Acute Kidney InjuryAntibodies, Monoclonal, HumanizedBrainBrain DiseasesComorbidityComplement ActivationComplement Pathway, AlternativeDisease OutbreaksGastroenteritisGermanyHemolytic-Uremic SyndromeHumansKidneyNervous System DiseasesPlasma ExchangeRenal Replacement TherapyAntibodies, Monoclonal, Humanizedeculizumab

Identifiers

PMID22986362
OpenAlexW2033118339

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.