Abstract
In 16 of 52 cases (32.5 per cent) of glomerulonephritis associated with glomerular subendothelial electron dense deposits, we detected endothelial endocytosis of osmiophilic material. Twelve patients had systemic lupus erythematosus, two had poststreptococcal glomerulonephritis, and two had idiopathic immune complex glomerulonephritis. The endocytosis was not observed in 13 patients suffering from membranoproliferative glomerulonephritis, in seven suffering from focal sclerosing glomerulonephritis, and in one suffering from hereditary nephritis. Therefore, the potential for endocytosis appeared to vary according to the illness. By light microscopy the 16 specimens exhibited features of acute proliferative glomerulonephritis. All the 14 with tissue sufficient for immunofluorescence study displayed deposition of immunoglobulins and complement along capillary loops and within the mesangium. By electron microscopy many of the subendothelial deposits were unassociated with endocytosis of osmiophilic matter, yet when endocytosis occurred, it was prominent. Hypertrophied endothelial cells occurred in zones of endocytosis. In nine of 16 cases small vacuoles within endothelial cells contained material of an electron density comparable to that of intramembranous and subendothelial deposits, but lyosomal degradation of the material was not noticed. There was frequent direct communication between osmiophilic material in capillary lumens, the subendothelial aspect of the glomerular basement membrane, and endothelial cytoplasmic processes. These communications suggested movement of osmiophilic material in some fashion. Neutrophils featuring vacuoles that contained osmiophilic material were only rarely observed, indicating that they may not assume a major role in degradation of deposits. Phagocytic activity of mesangial cells and nonresident monocytes was not studied. On the basis of our findings we propose that endothelial endocytosis of osmiophilic material might constitute a component of a transport mechanism or a digestive mechanism of glomerular immune deposits located in the subendothelial region.
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