Most studies on the pathophysiology of HSP have focused on the dysregulation of IgA production [9]: increased serum IgA levels, IgA-containing immune complexes which alter the vessels, presence of abnormal IgA1 glycosylation in renal disease, abnormalities in the regulation of clearance of IgA from the liver, and coagulation disorders (high d-dimer concentrations) [10–12]. This evidence concerns the gene CD79A and kidney disorder.