IGHA1 and glomerulonephritis: In contrast, IgA1 immune complexes in renal tissue were digested and broken down by renal cells with immunosuppressive treatment and time, and thus the level of monoclonal IgA2 in circulation and renal tissues gradually increased, demonstrating a transient dense deposit disease pattern on electron microscopy and progressive endocapillary proleferative glomerulonephritis with increasing interstitial fibrosis and tubular atrophy on light microscopy.