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American Journal of Pathology, Vol 122, 520-530, Copyright © 1986 by American Society for Investigative Pathology

REGULAR ARTICLES

No aggravation of the course of experimental glomerulonephritis in spontaneously hypertensive rats

HD Stein, RB Sterzel, JD Hunt, R Pabst and M Kashgarian

Functional and morphologic glomerular alterations induced by antiglomerular basement membrane (anti-GBM) nephritis were investigated in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto controls (WKY) for assessment of the role of systemic hypertension in immunologically mediated renal injury. Over a 6-week period serial measurements of systolic blood pressure (BP), serum creatinine (SCreat), creatinine clearance (CCreat), and urinary albumin excretion (UAlbV) were obtained with inulin clearances (CInulin) at the end of the study. Renal tissue was examined by light microscopy (LM), electron microscopy, immunofluorescence, flash 3H-thymidine autoradiography (AR), and staining for nonspecific esterase (NSE). Immunologic humoral response was evaluated by measurement of rat anti-rabbit IgG antibody production. At all time periods studied, SHR and WKY rats with anti-GBM nephritis demonstrated comparable elevations in SCreat and UAlb V as well as diminution of CCreat and CInulin as compared with non-nephritic control rats of each strain. In nephritic WKY rats mild hypertension developed, whereas in nephritic and control SHR rats marked elevations in BP developed. Morphologic injury as assessed by percent glomerular crescents and hypercellularity on LM, numbers of monocyte macrophages by NSE staining, immunofluorescence for IgG, C3, fibrinogen and Ia positivity, and numbers of glomerular 3H-thymidine-labeled cells by AR was notably comparable in both nephritic strains. Humoral antibody responses were also shown to be similar in all rats studied. These results demonstrate that the 5-week course of experimental anti-GBM nephritis is not exacerbated by systemic hypertension. Glomerular autoregulatory capacity may be important in determining the extent of immune-mediated renal injury.


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[Abstract] [Full Text] [PDF]


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Copyright © 1986 by the American Society for Investigative Pathology.