BackgroundHenoch-Schönlein Purpura (HSP) is a common small vessel vasculitis in children which is characterized by non-thrombocytopenic purpura, arthritis, bowel angina and glomerulonephritis [1]. It is generally accepted that immunoglobulin A (IgA), especially IgA1 and complement C3 deposited in the walls of arterioles, capillaries, and venules, immune inflammatory reaction are involved in the vascular endothelial cell injury of HSP patients [1-3]. In the majority of cases, HSP is a self-limiting disease and treatment is supportive. However, HSP has a high rate of recurrence, and some patients can progress to HSP nephritis (HSPN), which can result in renal failure [4]. Up to now, there is no effective therapy to impede these events to occur. So it is extremely urgent to further research on the pathophysiology of HSP.Acid-sensing ion channels (ASICs) are cationic channels which belong to the degenerin/ epithelial Na + channel (DEG/ENaC)