Hemolytic-uremic syndrome: Difference between revisions

Latest revision as of 13:29, 20 April 2023

Typical HUS is a thrombotic microangiopathy with prominent renal failure traditionally associated with Shiga toxin-producing Escherichia coli infection, especially enterohemorrhagic E. coli O157:H7
Different pathophysiology and treatment from atypical hemolytic-uremic syndrome and secondary hemolytic-uremic syndrome

Typical HUS is caused by Shiga toxin from enterohemorrhagic Escherichia coli (e.g. O157:H7)
Shiga toxin is absorbed systemically
- Damages vascular endothelial cells leading to cytokine release and thrombus formation
- Actives complement and binds Factor H (a complement regulator)

Abdominal pain and watery diarrhea about 4 days after exposure to toxin, progressing to bloody diarrhea with or without vomiting
- Up to one third do not have bloody diarrhea
- Fever is mild or absent
About 7 days after onset of diarrhea, HUS develops
- Progression of hemolytic anemia, thrombocytopenia, and severe AKI
Other preceding infections can include UTI, SSTI, or other causes of gastroenteritis

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 *Typical HUS is a [[thrombotic microangiopathy]] with prominent renal failure traditionally associated with Shiga toxin-producing [[Escherichia coli]] infection, especially enterohemorrhagic ''E. coli'' O157:H7
-*Difference pathophysiology and treatment from [[atypical hemolytic-uremic syndrome]]
+*Different pathophysiology and treatment from [[atypical hemolytic-uremic syndrome]] and [[secondary hemolytic-uremic syndrome]]
 ===Pathophysiology===
 *Typical HUS is caused by Shiga toxin from enterohemorrhagic [[Escherichia coli]] (e.g. O157:H7)
-*Toxin is absorbed systemically, causing platelet activation and aggregation
+*Shiga toxin is absorbed systemically
+**Damages vascular endothelial cells leading to cytokine release and thrombus formation
+**Actives complement and binds Factor H (a complement regulator)
 ===Risk Factors===