Background: Some allergic inflammation-associated mediators have been reported in acute stage of HenochSchönlein purpura (HSP). However, the association of children with allergic diseases and their subsequent risks of HSP and HSP nephritis remain unknown. Methods: In this study, we included 2,240 children with HSP diagnosed between 2000 and 2008 as well as 8,960 non-HSP controls matched for age, sex, and level of urbanization. The odds ratios (ORs) of HSP were calculated with respect to associations with pre-existing allergic diseases. results: Children with allergic diseases had an increased subsequent risk of HSP; the lowest adjusted OR (aOR) was 1.33 for allergic conjunctivitis (95% confidence interval (CI): 1.17-1.52) and the highest was 1.68 for asthma (95% CI: 1.48-1.91). The aOR increased to 2.03 (95% CI: 1.80-2.31) in children with at least two allergic diseases. Children who visited medical institutes more often per year for associated allergic diseases had an increased risk of HSP. Of the 2,240 children with HSP, 249 (11%) had HSP nephritis and 45.8% of those with nephritis had history of any allergic disease. conclusion: Atopic children had an increased subsequent risk of HSP but not an increased risk of HSP nephritis. h enoch-Schönlein purpura (HSP) is a common systemic small vessel vasculitis that primarily affects children and is characterized by nonthrombocytopenic purpura, abdominal pain and bleeding, arthritis, and renal involvement. Although the clinical course of HSP is generally benign and self-limited (1), renal function impairment, bowel perforation, and central nerve system involvement are rare but cause severe morbidity and long-term complication which need more aggressive treatment (1-3). HSP with renal involvement, HSP nephritis, has been reported to occur in 20-50% of the patients with HSP, and the long-term outcome of HSP depends primarily on the extent of renal involvement (4-7). The manifestations of HSP nephritis vary from asymptomatic hematuria and/or proteinuria to nephritic syndrome, nephrotic syndrome, and rapidly progressive glomerulonephritis (4-7). To date, the exact etiology and pathogenesis of HSP are unknown. However, HSP is regarded as a specific immune-mediated inflammation induced by environmental factors, such as infections and seasonal variation (1,8). Some inflammatory mediators, including tumor necrosis factor (TNF)-α, interleukin-6, IL-8, transforming growth factor (TGF)-β, vascular endothelial growth factor (VEGF), and cysteinyl leukotrienes, have been reported to be higher in children with acute HSP than in healthy controls (9-11). Cysteinyl leukotrienes are potent inflammatory mediators which contribute to asthma (12). Elevated Th2-mediated biological markers such as elevated serum IgE, serum eosinophil cationic protein (ECP), and urinary leukotriene E4 levels were found in acute stage of HSP (10-13). The onset of HSP has been reported after exposure to drug or food allergens, vaccines, and insect bites (14-16). In our clinical experience, some children with HS...