Hemolytic uremic syndrome: An updated review


  • Elmukhtar Habas Professor
  • Amnna Rayani Professor of pediatrics, Pediatric Hospital, Tripoli University, Tripoli-Libya
  • Ala Habas Medical Student
  • Kalifa Farfar Consultant physician
  • Ahmed El Marghani
  • Abdel-Naser Elzouki Professor of internal medicine




HUS, atypical HUS, Typical HUS, renal impairment, hemolysis, thrombocytopenia


Hemolytic uremic syndrome (HUS) is a microangiopathic thrombotic disease. HUS is classified into typical, secondary, and atypical types. All types are characterized by thrombocytopenia, acute kidney impairment, and hemolysis. Infection with Shiga toxin from Escherichia coli causes typical HUS. Atypical HUS is frequently caused by abnormal complement activation via the alternative pathway because of gene mutations or autoantibodies synthesis. Secondary HUS accompanies post-transplantation, autoimmunity, cancer, etc. Endothelial cell injury initiates cells destruction stimulates procoagulant state, which activates platelet and thrombus generation, producing ischemic tissue injury.

HUS pathogenesis is the result of an ineffective complement activation cycle that causes endothelial cells damage, activating platelet and thrombus formation. In some atypical HUS cases, interrupting the pathogenesis cycle of HUS by inhibiting complement activation might be beneficial, but not in those with gene mutations and patients with typical or secondary HUS. Hence, the pathogenesis of HUS types understanding is required; therefore, a comprehensive review of the differences and resemblances between the HUS types will be discussed and updated.


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How to Cite

Hemolytic uremic syndrome: An updated review. (2022). Yemen Journal of Medicine, 1(1), 6-13. https://doi.org/10.32677/yjm.v1i1.3346

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