Decreased ultrafiltration coefficient, LpA or Kf, was documented previously in micropuncture studies of glomerulonephritis in rats. Observations were made immediately following an injection of antiglomerular basement membrane (anti-GBM) antibody, later in the course of glomerulonephritis, and during the chronic phase of Heymann nephritis. To gain further insight into the basis of reduced glomerular filtration rate in immune-complex glomerulonephritis, we studied the anatomic, physiologic, and rheologic properties of isolated glomeruli from female Buffalo rats with nephritis which developed during infection with Trypanosoma rhodesiense. Immune-complex mediated glomerulonephritis was present 2 weeks after inoculation and progressed throughout the 4 weeks of study. Renal insufficiency occurred, with serum creatinine concentrations rising to 5 to 10 times control values by week 4. Mesangial hypercellularity, mesangial electron dense deposits, and endothelial cell swelling were observed. Increased numbers of mononuclear cells were present within the glomerulus. Total glomerular water volume was greater in nephritic than in normal animals. Increased cell volume accounted for most of the volume increment. When filtration into the capillaries was induced in vitro by imposing an oncotic gradient of 6.5 mm Hg or greater across the capillary wall, rapid and uniform erythrocyte movement occurred within the capillaries of control glomeruli and erythrocytes were ejected into the medium. In contrast, a transcapillary gradient of 30 to 40 mm Hg was required to produce erythrocyte movement in glomeruli from nephritic animals studied 4 weeks after inoculation. The ultrafiltration coefficient of nephritic glomeruli was estimated in vitro and was not different from that of control glomeruli (5.81 ± 0.35 vs. 6.21 ± 0.49 nl/ min mm Hg). An impairment of capillary perfusion may be responsible for the decreased rate of glomerular filtration observed in this model of glomerulonephritis.
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