Evidence map›Paper›PMID 41140828›Full record

ArticleNagoya journal of medical science2025

Atypical hemolytic uremic syndrome treated with anti-C5 antibody agent eculizumab, without genetic complement abnormalities.

Yuka Sato, Noritoshi Kato, Marina Asano, Hideaki Shimizu, Yoshitaka Tatematsu, Yuko Shimamura, Asuka Horinouchi, Kayaho Maeda, Sawako Kato, Tomoki Kosugi and 1 more

Abstract readCase Reports
In one paragraph

Article in Nagoya journal of medical science, 2025. 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

11 authors.

Yuka SatoDepartment of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Noritoshi KatoDepartment of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Marina AsanoMihama Clinic, Mihama, Japan.
Hideaki ShimizuDepartment of Nephrology, Daido Hospital, Nagoya, Japan.
Yoshitaka TatematsuDepartment of Nephrology, Fujita Health University Bantane Hospital, Nagoya, Japan.
Yuko ShimamuraDepartment of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Asuka HorinouchiDepartment of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kayaho MaedaDepartment of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Sawako KatoDepartment of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Tomoki KosugiDepartment of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shoichi MaruyamaDepartment of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atypical hemolytic uremic syndrome (aHUS) is a rare and life-threatening disease often complicated by end-stage renal disease. Anti-C5 antibody agents have been developed for the treatment of aHUS: these are highly effective but limited in use owing to the difficulty of diagnosing aHUS in the acute clinical phase. The pathophysiology of aHUS is a thrombotic microangiopathy (TMA) caused by complement dysregulation triggered by environmental factors in susceptible individuals with genetic factors. Although several germline variants associated with aHUS have been identified, approximately half of patients with aHUS lack known pathogenic variants. It is essential to recognize the characteristic clinical features of aHUS. These include the triad of hemolytic anemia, thrombocytopenia, and renal impairment, without the presence of Shiga toxin-producing

Indexed as

Antibodies, Monoclonal, HumanizedAtypical Hemolytic Uremic SyndromeComplement C5HumansAntibodies, Monoclonal, HumanizedComplement C5eculizumabanti-C5 antibodyatypical hemolytic uremic syndromecomplementeculizumabthrombotic microangiopathy

Identifiers

PMID41140828
PMCPMC12549117

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.