ReviewPediatric nephrology (Berlin, Germany)2010
Shiga toxin-associated hemolytic uremic syndrome: pathophysiology of endothelial dysfunction.
Review in Pediatric nephrology (Berlin, Germany), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 184 citations in OpenAlex.
- Hemolytic uremic syndrome: differential diagnosis with the onset of inflammatory bowel diseases.Acta bio-medica : Atenei Parmensis · 2018Pooled it
- Chronic sequelae of E. coli O157: systematic review and meta-analysis of the proportion of E. coli O157 cases that develop chronic sequelae.Foodborne pathogens and disease · 2014Pooled it
- Review
- Urgent Colectomy for Colonic Necrosis Following Shiga Toxin-ProducingSurgical case reports · 2026Article
- Molecular determinants of STEC-HUS: from complement activation to microvascular thrombosis.Frontiers in immunology · 2026Article
- P1PK blood group antigens in birds: implications for veterinary blood transfusion, human and pet health.BMC veterinary research · 2025Article
- Two cases of typical HUS in adults treated with an anti-C5 monoclonal antibody: a new perspective?Journal of nephrology · 2025Article
- INM004: Polyclonal Neutralizing Antibodies Against Shiga Toxin as a Treatment for Hemolytic Uremic Syndrome.Toxins · 2025Review
- Association ofFrontiers in cellular and infection microbiology · 2025Article
- EnterohemorrhagicFrontiers in cellular and infection microbiology · 2025Article
- Red blood cell-derived arginase release in hemolytic uremic syndrome.Journal of translational medicine · 2024Article
- The Role of the Complement System in the Pathogenesis of Infectious Forms of Hemolytic Uremic Syndrome.Biomolecules · 2023Review
- Cerebral microstructural changes in children suffering from hemolytic uremic syndrome.European journal of pediatrics · 2023Article
- Toll-like Receptor 4 in Acute Kidney Injury.International journal of molecular sciences · 2023Review
- Translocation of outer membrane vesicles from enterohemorrhagicFrontiers in microbiology · 2023Article
- Therapeutic Antibodies Against Shiga Toxins: Trends and Perspectives.Frontiers in cellular and infection microbiology · 2022Review
- Serum insulin-like growth factor-binding protein 2 levels as an indicator for disease severity in enterohemorrhagicRenal failure · 2021Article
- Primary Human Colon Epithelial Cells (pHCoEpiCs) Do Express the Shiga Toxin (Stx) Receptor Glycosphingolipids Gb3Cer and Gb4Cer and Are Largely Refractory but Not Resistant towards Stx.International journal of molecular sciences · 2021Article
- Article
- Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shiga toxin (Stx)-producing enterohemorrhagic Escherichia coli O157:H7 has become a global threat to public health, as a primary cause of a worldwide spread of hemorrhagic colitis complicated by diarrhea-associated hemolytic uremic syndrome (HUS), a disorder of thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure that mainly affects early childhood. Endothelial dysfunction has been recognized as the trigger event in the development of microangiopathic processes. Endothelial cells, mainly those located in the renal microvasculature, are primary targets of the toxic effects of Stx1 and 2. Stxs bound to their specific globotriaosylceramide (Gb3Cer) receptor on the cell surface trigger a cascade of signaling events, involving NF-κB activation, that induce expression of genes encoding for adhesion molecules and chemokines, and culminate in the adhesion of leukocytes to endothelial cells, thereby increasing the endothelial susceptibility to leukocyte-mediated injury. Activated endothelial cells in response to Stxs lose the normal thromboresistance phenotype and become thrombogenic, initiating microvascular thrombus formation. Evidence is emerging that complement activation in response to Stxs favors platelet thrombus formation on endothelial cells, which may play a role in amplifying the inflammation-thrombosis circuit in Stx-associated HUS.
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Registered trials
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.