Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy (TMA) characterized by the classic triad of microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and acute kidney injury (AKI). Typical HUS (90% of pediatric cases) is caused by Shiga toxin-producing Escherichia coli (STEC), most commonly serotype O157:H7. Shiga toxin binds to globotriaosylceramide (Gb3) receptors concentrated on renal glomerular endothelial cells, causing direct endothelial injury. Damaged endothelium exposes subendothelial collagen and tissue factor, triggering platelet adhesion, activation, and microthrombus formation in arterioles and capillaries. Red blood cells are mechanically sheared as they pass through partially occluded microvessels (fibrin strands), producing schistocytes (fragmented RBCs) — the hallmark of MAHA. Platelet consumption in microthrombi causes thrombocytopenia. Renal microthrombi cause glomerular ischemia and AKI. Atypical HUS (aHUS) is caused by dysregulation of the alternative complement pathway, most commonly from mutations in complement regulatory proteins (factor H, factor I, MCP/CD46) or autoantibodies to factor H. Uncontrolled complement activation on endothelial surfaces causes the same TMA pattern but without preceding diarrheal illness. aHUS has high mortality without treatment. Critical distinction: in typical STEC-HUS, antibiotics are CONTRAINDICATED (increase Shiga toxin release...