Evidence map›Paper›PMID 23733336›Full record

ArticleBlood2013

Quiescent complement in nonhuman primates during E coli Shiga toxin-induced hemolytic uremic syndrome and thrombotic microangiopathy.

Benjamin C Lee, Chad L Mayer, Caitlin S Leibowitz, D J Stearns-Kurosawa, Shinichiro Kurosawa

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Systematic review of atypical hemolytic uremic syndrome biomarkers.Pediatric nephrology (Berlin, Germany) · 2022
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Advances in our understanding of the pathogenesis of hemolytic uremic syndromes.American journal of physiology. Renal physiology · 2018
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. 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

5 authors.

Benjamin C LeeDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA.
Chad L Mayer
Caitlin S Leibowitz
D J Stearns-Kurosawa
Shinichiro Kurosawa

Funding

Translation of immunologic technologies from basic research into pre-clinical nonU19AI062629 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI THOMPSON, LINDA F · 2004 to 2023
$56.2M
Baboon Research Resource ProgramP40OD010988 · OD · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI BANKS, RON E · 2012 to 2018
$9.0M
Role of Inter-alpha Inhibitors in Anthrax IntoxicationR42AI062095 · NIAID · PROTHERA BIOLOGICS, LLC · PI OPAL, STEVEN M. · 2010 to 2012
$2.7M
PRIMATE MODEL AND PATHOGENESIS OF ANTHRAX SEPSISR01AI058107 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI KUROSAWA, SHINICHIRO · 2005 to 2009
$2.4M
NIAID NIH HHS R01 AI058107NIAID NIH HHS R01AI058107NIAID NIH HHS R42 AI062095NIAID NIH HHS R42AI062095NIAID NIH HHS U01 AI1075386NIAID NIH HHS U19 AI062629NIH HHS P40 OD010988NIH HHS P40OD010988
6 · The paper itself

Abstract

Enterohemorrhagic Escherichia coli (EHEC) produce ribosome-inactivating Shiga toxins (Stx1, Stx2) responsible for development of hemolytic uremic syndrome (HUS) and acute kidney injury (AKI). Some patients show complement activation during EHEC infection, raising the possibility of therapeutic targeting of complement for relief. Our juvenile nonhuman primate (Papio baboons) models of endotoxin-free Stx challenge exhibit full spectrum HUS, including thrombocytopenia, hemolytic anemia, and AKI with glomerular thrombotic microangiopathy. There were no significant increases in soluble terminal complement complex (C5b-9) levels after challenge with lethal Stx1 (n = 6) or Stx2 (n = 5) in plasma samples from T0 to euthanasia at 49.5 to 128 hours post-challenge. d-dimer and cell injury markers (HMGB1, histones) confirmed coagulopathy and cell injury. Thus, complement activation is not required for the development of thrombotic microangiopathy and HUS induced by EHEC Shiga toxins in these preclinical models, and benefits or risks of complement inhibition should be studied further for this infection.

Indexed as

AnimalsBlood CoagulationComplement ActivationComplement System ProteinsDisease Models, AnimalFibrin Fibrinogen Degradation ProductsHemolytic-Uremic SyndromePapioPrimatesShiga-Toxigenic Escherichia coliShiga ToxinThrombotic MicroangiopathiesTime FactorsComplement System ProteinsFibrin Fibrinogen Degradation Productsfibrin fragment DShiga Toxin

Identifiers

PMID23733336
PMCPMC3731933
OpenAlexW1984484335

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.