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Previous Volume 361:1676-1687 October 22, 2009 Number 17 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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The hemolytic–uremic syndrome is characterized by nonimmune hemolytic anemia, thrombocytopenia, and renal impairment.¹ The disorder occurs most frequently in children under the age of 5 years, with an annual incidence of 6.1 cases per 100,000 children under 5 years, as compared with an overall incidence of 1 to 2 cases per 100,000. The presentation is generally heralded by diarrhea, which is often bloody.^2,3 Most cases (including more than 90% of those in children) are secondary to infection with Escherichia coli serotypes O157:H7, O111:H8, O103:H2, O123, O26, or others,¹ which produce Shiga-like toxin (Stx), and several other bacteria, such as Streptococcus . . . [Full Text of this Article]

The Histologic Lesion

Classification of Disease

Familial Form

Sporadic Form

Complement Abnormalities

Genetic Abnormalities

Complement Pathway Mutations

Complement Factor H

CFH Point Mutations

Genomic Abnormalities

Autoantibodies against CFH

Membrane Cofactor Protein

CFI

CFB and C3

Thrombomodulin

Incomplete Genetic Penetrance

From Complement Abnormalities to Thrombotic Microangiopathy

Clinical Course and Outcome

Treatment

Transplantation

Evolving Approaches

Summary

Source Information

From the Clinical Research Center for Rare Diseases Aldo e Cele Daccò, Mario Negri Institute for Pharmacological Research (M.N., G.R.), and the Division of Nephrology and Dialysis, Ospedali Riuniti di Bergamo (G.R.) — both in Bergamo, Italy.

Address reprint requests to Dr. Remuzzi at the Mario Negri Institute for Pharmacological Research, Via Gavazzeni 11, 24125 Bergamo, Italy, or at gremuzzi@marionegri.it.

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