The mesangial cell in glomerulonephritis. I. Mechanisms of hypercellularity in experimental immune complex glomerulonephritis.
One-shot active immune complex glomerulonephritis was induced in rabbits by intravenous bovine serum albumin (250 mg. per kg.) and the mechanism of glomerular hypercellularity investigated. Most of the extra cells were mononuclear with few polymorphonuclear leukocytes. Fibrin was present in severe lesions. Glomerular mitoses were seen in normal kidneys but were more common in hypercellular glomeruli. This is direct evidence of local proliferation. Also, biopsies taken 1 hour after giving tritiated thymidine contained locally labeled cells. The mitotic rate and degree of local labeling both varied in proportion to the degree of hypercellularity. By electron microscopy both mesangial and endothelial cells were identified in mitosis. The majority of the mononuclear cells in the hypercellular glomeruli could not be identified by position or ultrastructure. Infiltration by nonglomerular cells was confirmed by the presence of macrophages, lymphocytes, and plasma cells.
D000818:Animals; D004195:Disease Models, Animal; D005921:Glomerulonephritis / Q000209:etiology / Q000473:pathology*; D007105:Immune Complex Diseases / Q000209:etiology / Q000473:pathology*; D007275:Injections, Intravenous; D007678:Kidney Glomerulus / Q000473:pathology / Q000648:ultrastructure; D008297:Male; D008938:Mitosis; D011817:Rabbits; D012710:Serum Albumin, Bovine / Q000009:adverse effects; D013936:Thymidine
D012710:Serum Albumin, Bovine; D013936:Thymidine