BOVINE SERUM-ALBUMIN (BSA) NEPHRITIS IN RATS .2. HISTOLOGICAL-FINDINGS AND COMPLEMENT ACTIVATION BY IMMUNE-COMPLEX IN SHR RATS

Abstract

A mesangiopathic form of glomerulonephritis was induced in spontaneously hypertensive (SHR) rats. Bovine serum albumin (BSA) was given i.v. to primed rats for 3 wk and they were unilaterially nephrectomized (Nx). They then received rabbit anti-BSA- (group A) or normal serum (group B) for 7 days, and half the rats were killed to obtain another kidney (ex [experiment] 1). The remainder were killed 2 wk later, and their kidneys were examined (ex 2). In Nx kidneys, the glomerular lesions were characterized by leukocyte accumulation in the capillary lumina and by deposition of rat IgG, rat C3 [complement component 3] and BSA both in the mesangial area and along the capillary walls. Glomeruli of ex 1 kidneys manifested varying degrees of hypercellularity in the mesangium; a few leukocyte accumulations in the capillary lumina were noted, and the immune deposits had deceased in the mesangium but not on the capillary walls. In ex 2 kidneys, mesangial hypercellularity was conspicuous. There were no remarkable histological differences between group A and B rats; in ex 1 and ex 2 kidneys of group A, rabbit IgG was closely associated with rat IgG or C3. Serological evalution revealed that the amount of circulating rat anti-BSA antibody was relatively small and that C3 was consumed by newly formed circulating immune complexes during BSA administration. Polymorphonuclear leukocyte binding assay revealed that complement fixation to the immune deposits occurred in vitro and that this activity was highest in tissue from Nx kidneys.