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The diagnosis of aHUS that is caused by inappropriate complement activation has become more critical because eculizumab, a humanized anti-C5 monoclonal antibody, has been shown to be an effective therapeutic modality[9] that has been approved for the treatment of aHUS patients in Europe and the United States. Recently, Fan and colleagues evaluated genotype-phenotype relationships in 10 Japanese patients with aHUS and identified potentially causative mutations in complement factor H, C3, membrane cofactor protein, and thrombomodulin in 8 of the patients.[10] However, the definitive diagnosis of inappropriate complement activation in aHUS patients is difficult because some patients show normal serum levels of complement components[11] and there selleck are a number of complement regulatory proteins, making it difficult to decide which complement regulatory protein is responsible for a particular patient developing aHUS. STEC-HUS is characterized by diarrhea accompanied by bloody Cyclopamine cell line stools. However, diarrhea may also be present in some aHUS cases. Diarrhea in aHUS can be a manifestation of ischemic colitis. In addition, enteritis that is not caused by STEC can trigger aHUS. Therefore, a diagnosis of STEC-HUS cannot be made based on symptoms alone, and the earlier nomenclature that used ��D+HUS�� to correspond with STEC-HUS and ��D-HUS�� to correspond with aHUS is not used at present.[11] The involvement BML-190 of Shiga toxins should be confirmed by stool culture, the direct detection of Shiga toxins, or the detection of anti-lipopolysaccharide-IgM antibodies. Conventionally, TTP has been diagnosed based on the classic pentad (microangiopathic hemolytic anemia, thrombocytopenia, labile psychoneurotic disorder, fever, and renal failure). However, the discovery of ADAMTS13 led to the finding that 60�C90% of patients with TTP have a marked reduction in the activity of ADAMTS13, to a level of