Evidence map›Paper›PMID 31198225›Full record

ArticleClinical kidney journal2019

An updated classification of thrombotic microangiopathies and treatment of complement gene variant-mediated thrombotic microangiopathy.

Christof Aigner, Alice Schmidt, Martina Gaggl, Gere Sunder-Plassmann

Abstract read
In one paragraph

Article in Clinical kidney journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Secondary thrombotic microangiopathy following lung transplantation: a multicenter European cohort study.Transplant international : official journal of the European Society for Organ Transplantation · 2026
    Article
  7. Observational
  8. Article
  9. The Phenomenon of Thrombotic Microangiopathy in Cancer Patients.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Review
  12. Review
  13. Lethal immunotoxicity in high-dose systemic AAV therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Review
  14. Article
  15. Article
  16. Frontiers in pediatrics · 2023
    Article
  17. Article
  18. Review
  19. Article
  20. Article
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.

Christof AignerDepartment of Medicine III, Division of Nephrology and Dialysis, Medical University of Vienna, Vienna, Austria.ORCID 0000-0001-6940-8010
Alice SchmidtDepartment of Medicine III, Division of Nephrology and Dialysis, Medical University of Vienna, Vienna, Austria.
Martina GagglDepartment of Medicine III, Division of Nephrology and Dialysis, Medical University of Vienna, Vienna, Austria.ORCID 0000-0003-3422-2245
Gere Sunder-PlassmannDepartment of Medicine III, Division of Nephrology and Dialysis, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-9253-9921

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Conditions presenting with signs of thrombotic microangiopathies (TMAs) comprise a wide spectrum of different diseases. While pathological hallmarks are thrombosis of arterioles and capillaries, clinical signs are mechanical haemolysis, thrombocytopenia and acute renal injury or neurological manifestations. The current classification of various syndromes of TMA is heterogeneous and often does not take the underlying pathophysiology into consideration. Therefore we propose a simplified classification based on the aetiology of different syndromes leading to TMA. We propose to categorize different TMA syndromes in hereditary and acquired forms and classify them based on the genetic background or underlying conditions. Of course, this classification is not always distinctly applicable in each case and from time to time reassessment of the established diagnosis is strongly recommended. The recommended treatment of TMA in the past was plasma exchange (PE). However, recently, the terminal complement inhibitor eculizumab became commercially available and has shown promising results in different open-label studies and case series. In our centre, first-line therapy is PE; however, patients are instantly switched to complement inhibitory therapy in case of treatment failure or intolerance.

Indexed as

acute kidney injuryatypical haemolytic uraemic syndromecomplement systemkidney diseasethrombotic microangiopathy

Identifiers

PMID31198225
PMCPMC6543965

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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.