Terminal complement inhibition in atypical haemolytic uremic syndrome: a single-centre experience.

ABSTRACT:

Background

Atypical hemolytic uremic syndrome (aHUS) is a rare thrombotic microangiopathy (TMA) caused by complement dysregulation, leading to microangiopathic anemia, thrombocytopenia, and acute kidney injury (AKI). Complement over activation typically results from genetic mutations in alternative pathway proteins. The genetic profile varies regionally and influences clinical phenotype and outcomes.

Methods

We conducted a retrospective observational study in all 27 patients (12 children, 15 adults) diagnosed with aHUS, at "Fundeni" Clinical Institute, between January 2017 and January 2025. Median age was 30 years (range, 1-70), 59% female. All patients were treated with anti-C5 monoclonal antibodies and followed for a median of 13 months (9-27).

Results

No patient ha

SUBMITTER: Mocanu VD 

PROVIDER: S-EPMC12665522 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature