Hemolytic uremic syndrome: An updated review

Abstract

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.

Volatile Fatty Acids Effective as Antibacterial Agents against Three Enteric Bacteria during Mesophilic Anaerobic Incubation

“…These organisms can become potentially pathogenic to humans when they find their way into soil and water environments through unsafe handling practices of human excrement and animal manure, such as the use of untreated faecal wastes as fertiliser, as these bacteria are transmissible through the faecal-oral route. The virulent strains could cause gastroenteritis or more fatal illnesses such as hemolytic uremic syndrome and pneumonia [18][19][20]. Furthermore, they have all been implicated as common causes of bacteremia in immunosuppressed people or patients undergoing invasive surgical procedures [21].…”