IGHA1 and hereditary spastic paraplegia: In parallel, abnormally glycosylated IgA1 molecules (hypogalactosylation and hyposialylation on the hinge region) observed in patients with IgAN and HSP is associated with the shedding of a soluble form of FcαRI (sFcαRI), which participates in the formation of circulating IgA1 complexes (95).