Effect of sodium cromoglycate on an experimental model of IgA nephropathy.

Recently, we reported on an experimentally-induced model of IgA nephropathy in mice, in which the lesions were very similar to those found in human IgA nephropathy. This model was achieved by long-term oral immunization and intravenous injection of colloidal carbon in order to achieve reticuloendothelial (RES) dysfunction. In this paper, we investigated the effects of sodium cromoglycate (SCG), an anti-allergic agent, on this model. Mice were treated with a small amount of colloidal carbon three times to block the RES, in addition to receiving oral administration of lactalbumin, as a food antigen. Open renal biopsy was performed at 18 weeks after the RES blockade, and mice were divided into 2 groups. One group received orally administered SCG and lactalbumin [SCG(+)], and the other group received lactalbumin only [SCG(-)] from 19 to 30 weeks. At 30 weeks, all mice were sacrificed for histopathological observation of renal tissue and blood sampling. IgA nephropathy had developed in all mice of the SCG(-) group, but had not developed in 7 out of the 9 mice in the SCG(+) group, at 30 weeks. Serum IgA levels obtained on sacrifice were significantly higher in the SCG(-) group. It was concluded that SCG effectively inhibited, not only the onset, but also the progression of IgA nephropathy in our original model. The effective mechanisms of this drug may act to suppress the local immunity produced through sensitization of gastrointestinal mucosa by food antigens.