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. 1988 Jun;131(3):411–417.

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

I Ogata 1, K Fujiwara 1, T Nishi 1, S Kuwata 1, Y Ohta 1, K Nosaka 1, H Oka 1
PMCID: PMC1880713  PMID: 3381876

Abstract

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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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