Children develop typical and atypical forms of HUS secondary to infectious pathogens (E. coli 0157:H7, Salmonella, Campylobacter, and Pneumococcus spp) [20–22], and underlying genetic defects such as deficiency in certain complement factors or proteins associated with processing the ultra-large thrombogenic multimers of vWF [23–25]. This evidence concerns the gene VWF and hemolytic-uremic syndrome.