GOLD NEPHROPATHY - TISSUE ANALYSIS BY X-RAY FLUORESCENT SPECTROSCOPY

Abstract

Three patients developed proteinuria following Au therapy for rheumatoid arthritis. The clinical syndrome was a self-limiting proteinuria with normal renal function. By light and EM appearances the renal lesion was an epimembranous deposit form of membranous glomerulopathy. Immunofluorescent study showed granular deposits of Ig[immunoglobulin]G and C3 complement along glomerular basement membranes. By X-ray fluorescent spectroscopic examination, Au was seen to be present within the proximal convoluted tubular cells but was not identified in the glomerular subepithelial deposits. These findings are consistent with an immune-complex form of glomerulopathy in which Au is neither the antigen nor a hapten in the glomerular deposits and suggest that the antibodies to tubular epithelial antigens induced by Au therapy may be a causative factor in the renal disease associated with Au therapy in rheumatoid arthritis.