This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ogata, I. Articles by Oka, H. Search for Related Content PubMed PubMed Citation Articles by Ogata, I. Articles by Oka, H.

American Journal of Pathology, Vol 131, 411-417, Copyright © 1988 by American Society for Investigative Pathology

REGULAR ARTICLES

Contribution of hepatic reticuloendothelial system to glomerular IgA deposition in rat liver injury

I Ogata, K Fujiwara, T Nishi, S Kuwata, Y Ohta, K Nosaka and H Oka
First Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.

Liver damage was induced in rats by a single dose of dimethylnitrosamine or D-galactosamine. In the dimethylnitrosamine model, marked glomerular IgA deposition occurred between Days 4 and 28, with its peak at Day 14. Serum IgA levels were significantly increased at Days 2 and 4, then gradually decreased, and normalized at Day 14. In the D-galactosamine model, however, no such deposition was observed, though serum IgA levels similarly increased on Days 2 and 4. IgA content in high molecular weight fraction from serum increased at Day 3 in both models. This increment remained at Day 7 only in the dimethylnitrosamine model, in which carbon clearance from the circulation was significantly decreased at Day 3. These data suggest that dysfunction of the hepatic reticuloendothelial system is a factor contributing to glomerular IgA deposition occurring in liver injury.