Gold nephropathy.
The early use of gold in medicine and dentistry dates back to the ancient Chinese and Egyptians. The discovery in 1890 that gold salts were toxic in vitro to tubercle bacilli led to the extensive treatment of tuberculosis with gold salts in the first three decades of this century. Eventually, gold therapy was extended to arthritis and lupus erythematosus, because of the belief that these diseases were forms of tuberculosis. Because of its beneficial effect particularly on active rheumatoid arthritis, chrysotherapy has remained one of the most widely used treatments of rheumatoid arthritis for the past half century. Toxicity of gold salts includes hypersensitivity reaction of skin and mucous membranes, bone marrow depression, and nephrotoxicity. The nephrotoxic clinical manifestations are renal insufficiency, proteinuria and hematuria, and the nephrotic syndrome. The pathologic changes are tubular degeneration, acute tubular necrosis or immune complex glomerulonephritis. The justification that any of these possible changes are the result of gold therapy rests clinically upon the time relationship of gold therapy and the renal symptoms, and pathologically upon the presence of gold inclusions (aurosomes) in proximal tubular epithelial cells. Aurosomes can at times be visualized by light microscopy, are usually seen by electron microscopy, and can be identified by microprobe analysis. Their pathology will be illustrated and pathogenic mechanisms discussed.
D001172:Arthritis, Rheumatoid / Q000188:drug therapy; D006046:Gold / Q000633:toxicity*; D006801:Humans; D007668:Kidney / Q000648:ultrastructure*; D007674:Kidney Diseases / Q000473:pathology*; D007678:Kidney Glomerulus / Q000648:ultrastructure; D007687:Kidney Tubules, Proximal / Q000648:ultrastructure; D008854:Microscopy, Electron; D014397:Tuberculosis, Pulmonary / Q000188:drug therapy
D006046:Gold