Evidence map›Paper›PMID 26974272›Full record

ReviewBone marrow transplantation2016

Post-bone marrow transplant thrombotic microangiopathy.

F Obut, V Kasinath, R Abdi

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Bone marrow transplantation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03384693 (A Pilot Trial of Using Pre-Transplant Risk Stratification and Prophylactic Defibrotide to Prevent Serious Thrombotic Microangiopathy in High-Risk Hematopoietic Stem Cell Transplant Patients), which is not on this map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 14% 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.

NCT03384693 phase2completednot on this mapstarted 2018, after this paper: background citation

A Pilot Trial of Using Pre-Transplant Risk Stratification and Prophylactic Defibrotide to Prevent Serious Thrombotic Microangiopathy in High-Risk Hematopoietic Stem Cell Transplant Patients

TypeinterventionalSponsorUniversity of California, San FranciscoRan2018 to 2020Enrolled25ConditionsThrombotic MicroangiopathiesArmsDefibrotide
3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Hemolytic Uremic Syndrome Associated WithMayo Clinic proceedings. Innovations, quality & outcomes · 2018
    Article
  9. Article
  10. Thrombotic microangiopathies: a general approach to diagnosis and management.CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne · 2017
    Review
  11. 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

3 authors at 1 institution in 1 country.

F ObutTransplantation Research Center, Department of Medicine, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
V KasinathTransplantation Research Center, Department of Medicine, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
R AbdiTransplantation Research Center, Department of Medicine, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Harvard University · US

Funding

TRAINING PROGRAM IN ACADEMIC NEPHROLOGYT32DK007527 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 1986 to 2021
$8.8M
NIDDK NIH HHS T32 DK007527
6 · The paper itself

Abstract

Thrombotic microangiopathy (TMA) is a systemic disease characterized by microangiopathic hemolytic anemia, thrombocytopenia and organ failure. Post-bone marrow transplant TMA (post-BMT TMA) is a life-threatening condition that has been reported to afflict between 0.5 and 63.6% of BMT patients. The incidence of post-BMT TMA is affected by evolving therapies such as conditioning regimens. The etiology of post-BMT TMA is thought to be multifactorial, including the effects of immunosuppressive agents, viral infections, TBI and GvHD. A growing body of evidence highlights the importance of complement system activation and endothelial damage in post-BMT TMA. Although plasmapheresis has commonly been used, its therapeutic rationale for the majority of post-BMT TMA cases is unclear in the absence of circulatory inhibitors. It has become possible to target complement activation with eculizumab, a drug that blocks the terminal complement pathway. Early studies have highlighted the importance of anti-complement therapies in treating post-BMT TMA. Moreover, finding complement gene mutations may identify patients at risk, but whether such patients benefit from prophylactic anti-complement therapies before BMT remains to be studied. This review focuses on diagnostic criteria, pathophysiology, treatment and renal outcomes of post-BMT TMA.

Indexed as

Bone Marrow TransplantationComplement ActivationEndothelium, VascularHumansKidney DiseasesPremedicationThrombotic Microangiopathies

Identifiers

PMID26974272
PMCPMC8647046
OpenAlexW2296648058

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.