HUS — anemia, low platelets, and kidney failure together. The STEC (E. coli) form in children, the atypical complement form in all ages, and why rapid recognition matters.
Evidence reviewed & updated: 2026-08 — reflects the latest published trials and guidelines.
Hemolytic uremic syndrome (HUS) is the dangerous triad of microangiopathic hemolytic anemia, low platelets, and acute kidney injury. Most cases follow E. coli O157 infections in children (STEC-HUS); the 'atypical' form (aHUS) is a complement-system disease that can strike anyone at any age and recurs without treatment. Rapid recognition and supportive care (or complement blockade in aHUS) are life-saving.
STEC-HUS follows Shiga-toxin-producing E. coli (most commonly O157) — classically after undercooked beef or contaminated produce — with bloody diarrhea, then the triad appearing about 1 week later. It's mainly a childhood disease and usually self-limited with supportive care, though severe AKI and death still occur.
Atypical HUS (aHUS) is a complement-system disease: uncontrolled complement activation attacks the microvasculature. It's genetic in ~60% (complement factor H, MCP, etc.) or antibody-mediated. It can present at any age, often after an infection trigger, and RECURS — without complement blockade, most patients progress or relapse.
The sequence is the clue: bloody diarrhea in a child, followed days later by pallor, bruising or petechiae, lethargy, and low urine output. Labs: anemia with schistocytes (fragmented red cells), low platelets, rising creatinine, low complement in aHUS.
The distinction STEC vs aHUS matters enormously: stool testing for E. coli O157/Shiga toxin first; if negative or if the patient is older, recurs, or has no diarrhea — think aHUS and test complement.
STEC-HUS is supportive: careful fluids, blood pressure control, dialysis when needed, and platelet transfusion only for bleeding (transfusing can worsen it). Antibiotics for E. coli O157 are generally avoided (may increase toxin release).
aHUS is treated with eculizumab — a complement C5 inhibitor that stops the attack, reversing anemia and platelets within days and frequently recovering kidney function. Plasma exchange bridges while awaiting diagnosis. With eculizumab, the outlook for aHUS transformed from poor to often recoverable — but treatment is typically lifelong.
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