Hemolytic-uremic syndrome: Difference between revisions

Revision as of 17:36, 20 August 2020

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

Typical HUS is caused by Shiga toxin from enterohemorrhagic Escherichia coli (e.g. O157:H7)
Toxin is absorbed systemically, causing platelet activation and aggregation

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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 ==Background==
-*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
+*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]]