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Plasma levels of C3d, which is liberated by enzymatic cleavage of C3, are determined in 97 patients with primitive chronic glomerular nephritis. This level is indicative of an abnormally high consumption of C3. In all cases where C3 is low, C3d is found at abnormally high levels. When the level of C3 is normal, C3d may, however, be elevated: a more subtle interpretation of the pathologic significance of C3 in immune disease is thus possible.

Measurement of serum C3 does not provide precise informations concerning an eventual consumption of this complement component during an immunological process. An increased synthetic rate may compensate an accelerated catabolism. The study of breakdown products of C3, such as C3d is a more sensitive approach of the role of complement in some immunological disorders. Therefore C3d was measured in the serum of patients with chronic non systemic glomerular diseases. High values of serum C3d were found in all cases of hypocomplementemic glomerulonephritis. Circulating C3d was also increased to a lower extent, in patients with normocomplementemic nephritis such as minimal change disease, mesangial nephritis with IgA deposits and membraneoproliferative (type I) glomerulonephritis. The data suggested the involvement of complement in a number of glomerulonephritis. Participation of complement in immunological disorders particularly in chronic non systemic glomerulonephritis could require a reevaluation when functional tests are performed in addition to static measurements.

A case of benign monoclonal gammapathy associated with an auto-immune hyperlipidaemia and a chronic glomerulopathy is reported. Extraction of the monoclonal immunoglobulin made it possible to demonstrate its anti-lipoprotein antibody activity. Parallel changes in serum lipid levels and monoclonal immunoglobulin levels under the influence of melphalan confirmed the direction relationship between the lipid and protein disorders. The pathogenesis of the glomerulopathy and of the massive and prolonged activation of the classical complement pathway is more difficult to affirm. It is nevertheless possible that the renal involvement is due to an auto-immune complex disease.