Abstract
BackgroundAtypical hemolytic uremic syndrome (aHUS) is a disorder of the microvasculature with hemolytic anemia, thrombocytopenia and acute kidney injury. Nowadays, aHUS is successfully treated with eculizumab, a humanized, chimeric IgG2/4 kappa antibody, which binds human complement C5 and blocks generation of C5a and membrane-attack-complex.Case presentationA 25-year-old woman with end stage renal disease due to relapsing atypical hemolytic uremic syndrome had a relapse of the disease during pregnancy. She was treated with eculizumab. We measured reduced formation of the membrane-attack complex in newborn’s umbilical cord vein blood using the sensitive and specific Palarasah-Nielsen-ELISA.ConclusionsEculizumab treatment of the mother with end stage renal disease may cause reduced innate immunity which could render newborns more susceptible to infections.
Highlights
Atypical hemolytic uremic syndrome is a disorder of the microvasculature with hemolytic anemia, thrombocytopenia and acute kidney injury
For this report we measured the deposition of complement C3 and C9 in the mother’s blood, in index newborn’s umbilical cord vein blood, and in blood 3 weeks after birth we measured deposition of complement C3 and C9 using the Palarasah-NielsenELISA as previously described [8, 9]
CH50 and AH50 methods are not based on ELISA principle but based on the spectrophotometric measurements of the degree of cell lysis following addition of antibody-sensitized sheep erythrocytes and sheep erythrocytes in solution, respectively
Summary
Eculizumab treatment of the mother with end stage renal disease may cause reduced innate immunity which could render newborns more susceptible to infections.
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