More detailed immunohistological and electron microscopic studies of renal pathology revealed distinct subgroups, namely those with a typical immune complex disease, with prominent deposits of immunoglobulin (Ig), MPGN, those without or only trace Ig but prominent deposits of C3 (now termed C3 glomerulopathy, C3G),27, 28 and a further subgroup of patients with electron dense deposits on glomerular and tubular basement membranes staining strongly for C3, the appropriately named dense deposit disease (DDD).29 This evidence concerns the gene C3 and primary membranoproliferative glomerulonephritis.