Hemolytic–uremic syndrome
A syndrome of kidney injury, low platelets, and red blood cell destruction.
Hemolytic–uremic syndrome (HUS) involves three main problems: a drop in red blood cells, acute kidney injury, and a low platelet count. Initial signs often include bloody diarrhea, fever, vomiting, and weakness. As the diarrhea continues, kidney issues and low platelets appear. Children get HUS more often than adults, and most children recover fully, though some face serious or life-threatening complications. In adults, especially the elderly, the condition tends to be more complex. Possible complications include neurological problems and heart failure.
Most cases follow an infection with a strain of *E. coli* known as O157:H7, but other triggers include *S. pneumoniae*, *Shigella*, *Salmonella*, and certain medications. The usual mechanism involves the bacteria producing Shiga toxin. A different form, atypical hemolytic uremic syndrome (aHUS), is often linked to a genetic mutation and has a different presentation. Both types can lead to widespread inflammation and multiple small blood clots in tiny vessels—a condition called thrombotic microangiopathy.
Treatment focuses on supportive care and may involve dialysis, steroids, blood transfusions, or plasmapheresis. About 1.5 out of every 100,000 people develop HUS each year. Fewer than 5% of those affected die. Among the survivors, up to 25% have ongoing kidney problems. The syndrome was first described in 1955.
**Signs and symptoms** After eating contaminated food, symptoms can appear 1 to 10 days later, typically after 3 to 4 days. Early signs include diarrhea (often bloody), stomach cramps, mild fever, or vomiting, which can lead to dehydration and reduced urine output. HUS usually develops 5 to 10 days after the first symptoms, but it can take up to 3 weeks, often appearing when the diarrhea is improving. Related signs include lethargy, decreased urine, blood in the urine, kidney failure, low platelets, and destruction of red blood cells (microangiopathic hemolytic anemia). High blood pressure, jaundice, seizures, and bleeding into the skin may also occur. Some people have noticeable neurological changes.
People with HUS often show signs of thrombotic microangiopathy (TMA), such as abdominal pain, low platelet count, elevated LDH (a marker of cell damage), low haptoglobin (indicating red blood cell breakdown), anemia, schistocytes (damaged red blood cells), high creatinine, protein in the urine, conf
- field
- Medicine
- known_for
- Characterized by low red blood cells, acute kidney injury, and low platelets; often caused by Shiga toxin-producing E. coli
- affected_population
- About 1.5 per 100,000 people per year
- mortality_rate
- Less than 5%
- first_defined
- 1955
Lore & Background
Hemolytic–uremic syndrome typically develops about 5–10 days after initial symptoms of infection, which can include bloody diarrhea, fever, vomiting, and weakness. The underlying mechanism involves Shiga toxin produced by bacteria such as E. coli O157:H7, which damages cells by binding to globotriaosylceramide (Gb3) receptors and inhibiting protein synthesis. This leads to widespread inflammation and multiple blood clots in small blood vessels, a condition known as thrombotic microangiopathy. Children have more Gb3 receptors than adults, which may explain their greater susceptibility.
Reader's Guide
Hemolytic–uremic syndrome is significant as a leading cause of acute kidney injury in children, though most recover without permanent damage. Its recognition as a distinct syndrome in 1955 helped clarify the link between infectious diarrhea and subsequent renal and hematologic complications. The condition highlights the role of Shiga toxin in triggering complement activation and thrombotic microangiopathy. Treatment remains supportive, including dialysis, steroids, blood transfusions, or plasmapheresis. While less than 5% of those affected die, up to 25% of survivors may have ongoing kidney problems. The syndrome also includes an atypical form often due to genetic mutation, which presents differently but shares the same underlying microangiopathic process.
Did You Know?
- HUS was first defined as a syndrome in 1955.
- Children are more commonly affected, possibly because they have more Gb3 receptors than adults.
- Less than 5% of those with HUS die, but up to 25% of survivors have ongoing kidney problems.
- Atypical hemolytic uremic syndrome (aHUS) is often due to a genetic mutation and presents differently from typical HUS.
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