Murine lupus nephritis. Effects of glucocorticoid on circulating and tissue-bound immunoreactants

We investigated the effects of methylprednisolone on immunoreactants of plasma and kidney to determine factors that might be relevant to the arrest of murine lupus nephritis. At the onset of nephritis, at about 5 months of age, the mice were divided in two groups and received either methylprednisolone or saline injections for 12 weeks. Before and after therapy (or saline injections), we determined the concentrations of plasma IgG, complement (C3), anti-DNA antibodies, Clq-reactive materials, creatinine, and urea nitrogen; in the kidneys, we assessed the relative distribution of IgG, IgM, and C3 in glomeruli, and we determined the concentration of IgG and anti-DNA activity of the eluted proteins. Our results indicated that methylprednisolone administered at the onset of nephritis preserved glomerular structure and function by decreasing the amount of tissue-bound immunoreactants and by inducing a preferential localization of immunoreactants in mesangia. Of the immunoreactants studied in plasma, a decreased concentration of IgG, but not the concentrations of anti-DNA antibodies, C3, and Clq-reactive materials, was associated with the arrest of nephritis. The anti-DNA activity in the renal eluates was very low and comparable in treated and untreated mice. Immune complex systems other than, or in addition to, DNA-anti-DNA likely play a role in the pathogenesis of murine lupus nephritis.