Typical HUS most commonly follows infection with Shiga toxin-producing Escherichia coli (STEC). Atypical HUS results from dysregulation of the alternative complement pathway. No causative genes or inheritance patterns are certified in this packet.

Diagnosis is based on clinical and laboratory identification of the defining triad: microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. No additional certified diagnostic criteria are documented in this packet.

No certified approved treatments are documented in this packet for hemolytic-uremic syndrome. Complement inhibition is the subject of active clinical investigation for atypical HUS. A Phase 3 trial evaluating crovalimab (NCT04861259, Hoffmann-La Roche) and a Phase 3 trial of iptacopan (NCT05795140, Novartis Pharmaceuticals) are currently active.

Prognosis is not certified in this packet.

Research is active across both typical and atypical HUS. An observational study tracking presentation and treatment outcomes in aHUS is ongoing (NCT06099236, AstraZeneca). A study investigating hyperhydration in children with STEC infection is recruiting (NCT05219110, University of Calgary). A new ravulizumab outcomes study in aHUS began recruiting in 2026 (NCT07399730, AstraZeneca). The published literature includes 270 classified articles, with case reports and reviews as the dominant types.