Abstract
Rats of Sprague-Dawley and two Wistar strains were injected fortnightly for 100 days with isolated human glomerular basement membrane emulsified in Freund's adjuvant and then slaughtered. Renal function was monitored by weekly urine protein estimations, and kidneys taken by unilateral nephrectomy and at slaughter were examined by light and electron microscopy and by immunofluorescence. Proteinuria began after 4 wk in Sprague-Dawley rats and continued until slaughter. Glomerular lesions, ranging from focal cellular proliferation and hypertrophy to widespread adhesions and sclerosis, were seen in these rats. By contrast, rats of both Wistar strains failed to develop proteinuria and no glomerular lesions were found. Sections stained with fluorescein-tagged anti-rat IgG antibody revealed intense and consistent linear fluorescence characteristic of anti-glomerular basement membrane antibody along the glomerular capillary walls of Sprague-Dawley rats. Such staining was either weak or absent in the other rats. This observed strain difference in susceptibility to experimental autologous antiglomerular basement membrane antibody glomerulonephritis is thought to be due to genetic variation in the capacity to produce antibody against the introduced foreign glomerular basement membrane.
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