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).
D000818:Animals; D000936:Antigen-Antibody Complex; D001172:Arthritis, Rheumatoid / Q000188:drug therapy; D001323:Autoantibodies; D001327:Autoimmune Diseases; D001485:Basement Membrane / Q000187:drug effects / Q000276:immunology; D005260:Female; D005921:Glomerulonephritis / Q000139:chemically induced* / Q000276:immunology; D006052:Gold Sodium Thiomalate / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D007105:Immune Complex Diseases / Q000139:chemically induced*; D007678:Kidney Glomerulus / Q000187:drug effects / Q000276:immunology*; D007684:Kidney Tubules / Q000187:drug effects / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011817:Rabbits; D051381:Rats
D000936:Antigen-Antibody Complex; D001323:Autoantibodies; D006052:Gold Sodium Thiomalate