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. 2018 Mar 19;293(19):7195–7208. doi: 10.1074/jbc.RA118.002639

Table 1.

Etiology of abnormalities in the alternative complement pathway in TMA

aHUS is caused by mutations in complement protein genes or from the development of autoantibodies directed against FH. TA-TMA is associated with post-bone marrow transplant environmental stressors. CFHR1/CFHR3 indicate the deletions of complement factor H-related genes 1 and 3.

aHUS, mutations in complement genes TA-TMA, environmental risk factors
Gain of function Immunosuppressive drugs
    C3 Total body irradiation
    CFB High-dose chemotherapy–conditioning regimens
Loss of function Graft versus host disease
    CD46 Infection
    THBD ABO incompatibility
    CFI Donor type
    CFH
    CFHR1/CFHR3 (deletion; plus autoantibody to FH)