Atypical hemolytic uraemic syndrome is caused by defects in the regulating factors in the alternative pathway of the complement system. Triggering can cause an uncontrolled complement activation with endothelial damage and thrombotic micro-angiopathy, especially in the kidneys. This can result in endstage renal failure. Complement activation during hemodialysis has been described as a result of contact between blood and the dialysis membrane. Our hypothesis is that patients with atypical hemolytic uraemic syndrome have a stronger complement activation during hemodialysis than patients with another underlying kidney disease. This could be a reason to treat patients with endstage renal failure due to atypical hemolytic uraemic syndrome preferentially with peritoneal dialysis instead of hemodialysis.
Study Type
OBSERVATIONAL
Enrollment
25
University Hospital Ghent
Ghent, Belgium
C3a-des-Arg measuring (as a marker of activation).
Time frame: at time 0, at 15 minutes, at 60 minutes and at 180 minutes
white blood cell count
Time frame: before and after 15 minutes of hemodialysis
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