Hemolytic Uremic Syndrome

Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy: small-vessel endothelial injury leads to platelet-rich microthrombi, especially in the renal circulation. As red blood cells squeeze through these narrowed, damaged vessels, they fragment into schistocytes. Platelets are consumed at the sites of clot formation, and reduced renal perfusion produces acute kidney injury. That single mechanism explains the defining triad: - microangiopathic hemolytic anemia; - thrombocytopenia; and - acute kidney injury. Typical HUS most often follows infection with Shiga-toxin-producing *Escherichia coli* (STEC), commonly after diarrheal illness that may be bloody. Shiga toxin injures the intestinal and renal endothelium. A patient can therefore arrive first with diarrhea and dehydration, then develop pallor, falling urine output, and rising creatinine as the microangiopathy evolves. Atypical HUS (aHUS) has a different driver: inherited or acquired dysregulation of the complement alternative pathway. Complement activation damages the endothelium and sustains the microvascular process. The distinction matters because typical HUS is usually managed supportively, whereas suspected aHUS may require early complement inhibition.