These results are consistent with complement protein deficiencies observed in diseases linked to FH mutations such as aHUS, glomerulopathies, and acute infections (C3: 5–68% and FB: 35–100% of normal (Nielsen et al., 1989; Vogt et al., 1995; Rougier et al., 1998)), where FH levels or function vary from 0 to 40% of normal levels. This evidence concerns the gene CFB and hyperinsulinemic hypoglycemia, familial, 4.