It has been postulated that IgA NP is caused by mesangial deposition of IgA-containing immune complexes formed by IgA polymers (pIgA) which are overproduced in response to antigens presented at mucosal surfaces. The intestinal mucosa is one possible source of this pIgA. To test whether antibodies to dietary antigens might be involved in the pathogenesis of IgA NP, we measured IgG and IgA serum antibody activities to gluten, a gluten fraction called glyc-gli, alpha-lactalbumin, beta-lactoglobulin, casein and ovalbumin in 54 patients with IgA NP by an enzyme-linked immunosorbent assay (ELISA). The IgA activities to gluten antigens and alpha-lactalbumin were significantly increased in IgA NP compared with a group of 40 age-matched healthy controls. In a previous study we found that 4 out of 12 patients with IgA NP and gastrointestinal complaints had subtotal villous atrophy; this indicated that many patients with IgA NP have altered intestinal permeability which may lead to activation of their intestinal immune system. Taken together our results showed a relation between the intestinal humoral immune system and IgA NP and indicated that antibodies to dietary antigens in some patients may be directly involved in the pathogenesis of IgA NP.