Mercury-induced autoimmune glomerulonephritis in inbred rats. II. Immunohistopathology, histopathology and effects of prostaglandin administration.

The repeated administration of mercuric chloride to BN rats induces the production of anti-GBM. In the present paper, we describe the immunohistopathology and histopathology of the kidneys from mercuricchloride-treated rats. Direct immunofluorescence demonstrated bright linear deposits of immunoglobulins at the level of the GBM of the kidney. Light microscopy failed to reveal substantial glomerular changes, but electron microscopy demonstrated a spectrum of ultrastructural alterations of the glomeruli (including the detachment of endothelial cells from the GBM and the presence of electron-opaque deposits). In the aggregate, these findings are suggestive of membranous glomerulonephritis. We also investigated whether treatment with low doses of PG had any effect on the course of this experimental model of autoimmune renal disease. Two groups of mercuric-chloride-treated BN rats received different doses of DMPGE2. This resulted in significantly lower levels of circulating autoantibodies to the GBM, as well as a decrease in the amounts of rat immunoglobulins bound to the kidneys and an increase in proteinuria. On the other hand, there were no major differences in renal histopathology between rats treated with DMPGE2 and controls.