| pubmed-article:7302364 | pubmed:abstractText | This work examines the cellular reaction in glomeruli of rats with an acute form of anti-glomerular basement membrane (GBM) nephritis. After intravenous injection of rabbit-derived anti-GBM serum, heterologous and, later, autologous IgG fixed to the glomerular capillary loops. From day 1 to 11 of nephritis, glomerular hypercellularity was not appreciable or modest by qualitative histology, whereas morphometric evaluation revealed mild but significant increases of glomerular cell counts as compared to untreated controls. Histoautoradiographic studies of renal tissue 2 h after pulse administration of 3H-thymidine served to determine the proportion of glomerular cells which synthesized DNA, indicating forthcoming cell division. The mean labeling index (LI) of epithelial cells of Bowman's capsule was 1.8% in controls, rose 4- to 5-fold on the first day of nephritis and fell gradually from day 2 to 11. LI to tuft cells was 1.9% in controls, peaked on day 4, and fell thereafter. Histochemical staining for nonspecific esterase, a marker of monocytes and macrophages, revealed that glomeruli of normal rats contain very few stained cells (mean: 0.2/tuft section). In the course of nephritis, a gradual increase of esterase-positive cells took place in glomeruli which reached a plateau on day 4 (mean: 5.5/tuft section), indicating an influx of migrating monocytes. It is concluded that the injury of this model of anti-GBM nephritis involves markedly enhanced proliferation of intrinsic glomerular cells associated with infiltration of monocytes. Such a prominent cellular response is revealed by the applied quantitative methods in the absence of histologically impressive glomerular hypercellularity. | lld:pubmed |
