The complement components CH50, C3, C4, and C1q, factor B, nephritic factor (NF), and circulating immune complexes (CIC) have been studied in 22 patients with chronic mesangiocapillary glomerulonephritis (CMCGN). Of the 22 patients studied, eight had normal complement levels and 14 had hypocomplementemia with marked reductions of C3 and CH50. Of the latter 14 patients, nine disclosed an activation pattern that followed the alternate pathway, while in the other five the classical pathway was followed. The patients with hypocomplementemia following the alternate pathway and with positive NF activity (five cases) had a histologic pattern of type II CMCGN with dense deposits within the basal membrane, while those with hypocomplementemia following the classical pathway and negative NF activity disclosed a histologic pattern of type I CMCGN. The etiopathogenesis of these two types of glomerulonephritis remains to be elucidated. Although the presence of CIC is discussed and they are only rarely detected with the usual techniques, immune complexes have been implicated as possible responsible factors in these diseases. It has been demonstrated that the NF is an IgG with the characteristics of an autoantibody specific against the C3bB and C3bBb convertases of the alternate pathway, thus forming the trimolecular complex C3bBbNF. Because serum NF is frequently associated to type II CMCGN, it could be speculated that this trimolecular complex behaves as an immune complex, the convertase C3b beeing the antigen and the NF, the antibody, and that, under certain circumstances and because of its low molecular weight, it could cause nephritis by its deposit in the glomerular basal membrane.