Evidence map›Paper›PMID 40766815›Full record

ArticleBlood vessels, thrombosis & hemostasis2024

Characterizing the association between complement-mediated TMA and cognitive dysfunction using MRI and neurocognitive assessment.

Pauline K Kosalka, Fahad Hannan, Jeff Hamilton, Christopher J Patriquin, Katerina Pavenski, Michael T Jurkiewicz, Leandro Tristao, Adrian M Owen, Sean C L Deoni, Jean Théberge and 5 more

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In one paragraph

Article in Blood vessels, thrombosis & hemostasis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Pauline K KosalkaDivision of Nephrology, Department of Medicine, Western University, London, ON, Canada.
Fahad HannanDepartment of Medical Biophysics, Western University, London, ON, Canada.
Jeff HamiltonDepartment of Medical Biophysics, Western University, London, ON, Canada.
Christopher J PatriquinDivision of Hematology, University Health Network, Toronto, ON, Canada.
Katerina PavenskiDepartment of Laboratory Medicine, St. Michael's Hospital, Toronto, ON, Canada.
Michael T JurkiewiczDepartment of Medical Imaging, Western University, London, ON, Canada.
Leandro TristaoDepartment of Medical Imaging, Western University, London, ON, Canada.
Adrian M OwenDepartment of Clinical Neurological Sciences, Western University, London, ON, Canada.
Sean C L DeoniAdvanced Baby Imaging Laboratory, Rhode Island Hospital, Providence, RI.
Jean ThébergeDepartment of Medical Biophysics, Western University, London, ON, Canada.
Jennifer MandziaDepartment of Clinical Neurological Sciences, Western University, London, ON, Canada.
Jonathan D ThiessenDepartment of Medical Biophysics, Western University, London, ON, Canada.
Jocelyn S GarlandDivision of Nephrology, Department of Medicine, Queen's University, Kingston, ON, Canada.
Susan B McGrathDivision of Nephrology, Department of Medicine, Western University, London, ON, Canada.
Shih-Han Susan HuangDivision of Nephrology, Department of Medicine, Western University, London, ON, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement-mediated thrombotic microangiopathy (CM-TMA) is a rare, life-threatening thrombotic microangiopathy caused by a defect in the alternative complement pathway. It is associated with renal failure and acute encephalopathy, but long-term neurocognitive effects are uncertain. Using magnetic resonance imaging (MRI) and neurocognitive tests, we can further evaluate the long-term neurocognitive complications in CM-TMA and compare them with controls. In this study, we analyzed microstructural changes in the cerebral white matter and neurocognitive testing results of patients with CM-TMA. Seven adult patients with CM-TMA in remission and 6 healthy controls were included. All patients were treated with C5 complement blockade. They were followed-up for 12 months after study entry. All patients had consecutive MRI scans (standard-of-care and quantitative sequences) to assess for white matter changes and concurrent neurocognitive testing. Patients with CM-TMA had increased white matter signal intensity in most regions of the brain compared with controls. This was accompanied by increased depression and neurocognitive dysfunction (impaired concentration, short-term memory, and verbal memory). These findings were also present up to 12 months after the initial study visit. In summary, patients with previous CM-TMA were found to have significant, albeit nonspecific, cerebral white matter abnormalities, with impaired memory and concentration. Larger studies with longitudinal follow-up to assess neurocognitive complications in CM-TMA are required. This trial was registered at Clinical Trials Ontario (ctontario.ca; project ID: 1318).

Identifiers

PMID40766815
PMCPMC12320465

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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.