20/01/2026
| InSide Davidson's | | HUS
Hemolytic Uraemic Syndrome
âPathophysiology and Presentation:
HUS is a form of thrombotic microangiopathy that primarily affects the renal microcirculation, though severe cases can involve other organs like the brain. It is characterized by the sudden onset of acute kidney injury (AKI), and in developed countries, it is the most common cause of AKI in children.
âCommon Infectious Etiology:
Most cases are caused by organisms that produce Shiga-like toxins (verotoxins), most notably enterohaemorrhagic Escherichia coli (serotype O157:H7) and Shigella dysenteriae. These toxins bind to receptors on microvascular endothelial cells after being contracted through contaminated food, water, or infected individuals.
âAtypical (Complement-Mediated) HUS:
In the absence of bloody diarrhea, "atypical" causes should be considered, which often involve abnormalities or genetic mutations in the complement system (e.g., CFH, CFI, MCP). Sporadic atypical cases may also be associated with autoantibodies to complement factor H.
âManagement Strategies:
While no specific treatment accelerates renal recovery for typical HUS, management focuses on supportive care and temporary renal replacement therapy (RRT) if needed. For complement-mediated HUS, management includes plasma exchange to replace complement components and remove autoantibodies.
âAdvanced Targeted Therapy:
Impressive results for treating complement-mediated HUS have been reported using eculizumab, an anti-C5 monoclonal antibody. It works by binding to C5 and preventing the activation of the terminal complement cascade.
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