Evidence map›Paper›PMID 18215115›Full record

ReviewAnnual review of pathology2008

Pathogenesis of thrombotic microangiopathies.

X Long Zheng, J Evan Sadler

Open access · greenAbstract readReview
In one paragraph

Review in Annual review of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 210 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Folate Deficiency-Induced Pseudo-Thrombotic Microangiopathy.European journal of case reports in internal medicine · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Thrombotic microangiopathy in patients with sickle cell disease.Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

23 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

2 authors at 2 institutions in 1 country.

X Long ZhengDepartment of Pathology and Laboratory Medicine, The Children's Hospital of Philadelphia and The University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA. zheng@email.chop.edu
J Evan Sadler
Children's Hospital of Philadelphia · USWashington University in St. Louis · US

Funding

THE ROLE OF SEMA4D/CD100 AND ITS RECEPTORS IN PLATELET BIOLOGY AND THROMBOSISP50HL081012 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI BRASS, LAWRENCE · 2006 to 2010
$11.9M
VON WILLEBRAND FACTOR MULTIMER ASSEMBLY AND STRUCTURER01HL072917 · NHLBI · WASHINGTON UNIVERSITY · PI SADLER, J EVAN · 2003 to 2012
$4.4M
Regulation of ADAMTS13 ActivityR01HL089746 · NHLBI · WASHINGTON UNIVERSITY · PI SADLER, J EVAN · 2007 to 2011
$2.1M
Structure and Function of ADAMTS13 MetalloproteaseR01HL079027 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI ZHENG, X. LONG · 2005 to 2009
$1.6M
NHLBI NIH HHS HL079027NHLBI NIH HHS HL72917NHLBI NIH HHS HL89746NHLBI NIH HHS P50 HL081012NHLBI NIH HHS P50HL081012NHLBI NIH HHS R01 HL072917NHLBI NIH HHS R01 HL079027NHLBI NIH HHS R01 HL089746
6 · The paper itself

Abstract

Profound thrombocytopenia and microangiopathic hemolytic anemia characterize thrombotic microangiopathy, which includes two major disorders: thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS). TTP has at least three types: congenital or familial, idiopathic, and nonidiopathic. The congenital and idiopathic TTP syndromes are caused primarily by deficiency of ADAMTS13, owing to mutations in the ADAMTS13 gene or autoantibodies that inhibit ADAMTS13 activity. HUS is similar to TTP, but is associated with acute renal failure. Diarrhea-associated HUS accounts for more than 90% of cases and is usually caused by infection with Shiga-toxin-producing Escherichia coli (O157:H7). Diarrhea-negative HUS is associated with complement dysregulation in up to 50% of cases, caused by mutations in complement factor H, membrane cofactor protein, factor I or factor B, or by autoantibodies against factor H. The incomplete penetrance of mutations in either ADAMTS13 or complement regulatory genes suggests that precipitating events or triggers may be required to cause thrombotic microangiopathy in many patients.

Indexed as

Acute Kidney InjuryADAM ProteinsADAMTS13 ProteinDiarrheaHemolytic-Uremic SyndromeHumansMicrocirculationPoint MutationPurpura, Thrombotic Thrombocytopenicvon Willebrand FactorADAM ProteinsADAMTS13 ProteinADAMTS13 protein, humanvon Willebrand Factor

Identifiers

PMID18215115
PMCPMC2582586
OpenAlexW2117019199

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.