It has been well known that renal functions are disturbed in patients with prolonged hepatobiliary disease but its pathogenesis is not yet defined. In order to disclose its pathogenesis, experimental hepatic injury was induced by intraperitoneal
administration of N-dimethylnitrosamine or D-galactosamine to rats. On immunohistochemical and ultrastructural study. It was observed that immunoglobulin was deposited on renal glomeruli of the rats.
@ES The results obtained were as follows.
@EN 1) In the N-dimethylnitrosamine-treated rats, there were necrotic spaces containing debris of necrotic hepatocytes and sinusoidal lining cells in the centrilobular areas 5 days after administration.
2) In the D-galactosamine treated rats, spotty necrosis with inflammatory cell infiltration throughout the lobule, and swelling and increment of Kupffer cells were appeared 2 days after administration.
3) There were slightly thickening of renal glomerular basement membrane and widening of the mesangeal matrix in N-dimethylnitrosamine-treated rats. 14 days after administration but no pathological changes were observed in glomerular basement
membrane
and mesangeal matrix in D-galactosamine-treated rats.
4) There were glomerular IgA deposition after administration of N-dimethylnitrosamine Slight deposits of IgA appeared 2 days after administration. In 5 days after administration, the deposits gradually intensified and peaked at 14 days after
administration. However, in the D-galactosamine-treated rats, only slight deposits of IgA appeared at days 7 and 14. There were no deopsitions of IgG in the N-dimethylnitrosamine or D-galactosamine treated rats.
5) On the ultrastructural study of the liver, degenerative change was most prominent at 7 and 14 days after administration of N-dimethylnitrosamine and D-galactosamine, respectively.
6) On the ultrastructural study of the kidney, most prominent change was noted at 7 days administration of N-dimethylnitrosamine or D-galactosamine.
From the above findings of immunohistochemical stain and electron microscopy, this study revealed that IgA was deposited on renal glomerular mesangium of the rats as a results of experimental hepatic injury induced by N-dimethylnitrosamine and
N-galactosamine. Also severe hepatic injury resulted in increase of plasma IgA level due to inhibition of excretion of polymeric IgA and immune complex through hepatobiliary tract, therefore this change indicated that IgA could be deposited on
renal
glomerular mesangium.
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