Studies have identified children with HSP exhibiting a reduced sialic acid component in the IgA1 heavy chain hinge region, activation of alternative pathways of complement, and alterations of the galactose content of oligosaccharide-linked IgA1 glycosylation, which can affect clearance of IgA and lead to mesangial deposition [3,5,8]. This evidence concerns the gene CD79A and hereditary spastic paraplegia.