In the urine and plasma of patients with FSGS, activated fragments of the complement cascade, such as C3a, C3b, Ba, Bb, C4a, and sC5b-9, are increased compared to patients with other renal diseases such as antineutrophilic cytoplasmic antibody (ANCA) vasculitis and lupus nephritis or in healthy controls (48). This evidence concerns the gene CFB and kidney disorder.