The pathogenesis of IgA nephropathy originates from Gd-IgA1 produced by mucosa-associated B cells, delayed-release budesonide directly reduces the production of pathogenic Gd-IgA1 at its source by inhibiting the activation and differentiation of B cells in the intestinal-associated lymphoid tissue, thereby achieving etiological treatment of the disease. Here, IGHA1 is linked to IgA glomerulonephritis.