Hypothesis for the pathogenesis of sodium aurothiomalate (Myocrisin) induced immune complex nephritis.

Renal complications associated with gold salt treatment in rheumatoid arthritis occur in fewer than 5% of treated patients. Recent investigations have shown that the renal lesion manifested clinically as membranous glomerulonephritis is caused by immune complexes. This paper presents a hypothesis for the mechanism by which gold causes this lesion: autoimmunization due to released tubular antigen(s). This hypothetical mechanism is strikingly similar to that responsible for autologous autoimmune nephrosis in the rat (Heymann's nephritis).