In order to determine the influence of
hypertension on the progression of chronic
glomerulonephritis, we studied the renal lesions in
Heymann nephritis (autologous
immune complex nephritis) produced in SHR. Nephritic SHR treated by AHD, normal SHR, nephritic WKYR, and normal WKYR served as controls. Induction of
Heymann nephritis did not alter the blood pressure in either SHR or WKYR as compared with each untreated control group. Administration of AHD normalized the blood pressure of SHR.
Proteinuria,
hypoproteinemia,
hypercholesterolemia, and reduction in
body weight were significantly greater in nephritic SHR than in nephritic SHR treated by AHD or nephritic WKYR, whereas BUN and serum
creatinine were unchanged in all the nephritic rats. Histological findings such as glomerular basement membrane thickening,
IgG and C3 deposits along capillary walls, and subepithelial electron-dense deposits were similar in all nephritic groups. Glomerular
sclerosis and tubulointerstitial changes were more marked in nephritic SHR than in the other nephritic groups. Severe vascular thickening and
necrosis, intravascular
thrombosis, and perivascular cell infiltration were frequently observed in nephritic SHR. These lesions are characteristic of
malignant hypertension. However, they were not found in control SHR, which maintained elevation of blood pressure equivalent to that of nephritic SHR throughout the study. It was concluded that
hypertension may aggravate nephritic manifestations such as
proteinuria,
hypoproteinemia, and
hypercholesterolemia but not excretory renal function and that the hypertensive vascular lesions are augmented by
Heymann nephritis.