It is commonly stated that mucosal immunity plays a role in the pathogenesis of IgA nephropathy (IgAN); however, the search for specific eliciting factors has been largely inconclusive. A dysregulated mucosal immune system with defective immune tolerance to commonly encountered pathogens or alimentary components is likely to be the key factor in triggering IgAN. Most of the interest, particularly in Asia, was being focussed on the possibility of modulating the mucosal immune system by tonsillectomy, a simple way of eradicating a source of pathogens, meanwhile reducing mucosal-associated immune system (mucosal-associated lymphoid tissue, MALT), but results are still inconclusive. Over the last years, a resurgence of interest has addressed the role of intestinal immunity facing dietary components, like gluten or the complex intestinal flora, the microbiota. The latter is focussing particular interest in recent reports, because it can vary according to diet and environmental factors, is modulated by the host genes and influences, in return, the MALT activity. Some data suggest a tempting new hypothesis for a strong intestine–kidney connection in IgAN. A defective immune tolerance might favour an abnormal response to microbiota with alterations of the intestinal barrier, including increased alimentary antigens and bacterial toxins absorption, triggering MALT activation and subclinical intestinal inflammation. This can produce abnormal response to alimentary antigens or commensal microbes with synthesis of aberrantly glycosylated polymeric IgA1 which eventually enter the circulation with renal deposits formation. The hypothesis is tempting also because it offers new treatment options, targeted to subclinical intestinal inflammation or microbiota modifications.