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The proportion of B lymphocyte subsets with surface immunoglobulin G (sIgG) was significantly increased in minimal change nephrotic syndrome (MCNS), membranous nephropathy, IgA nephropathy and mesangiocapillary glomerulonephritis (MCON) and with sIgA in IgA nephropathy and MCGN, and with sIgE in MCNS. Increased subsets in membranous nephropathy, IgA nephropathy and MCGN corresponded to the immunoglobulins deposited in the glomeruli, and the increased subset of sIgE in MCNS was correlated with the elevation of serum IgE. These results suggest that each disease studied has a characteristic subset pattern of B lymphocyte response. This may have an important rote in determining the histological type of idiopathic glomerulonephritis. [ABSTRACT FROM AUTHOR]

Thirty-two adult patients with minimal change nephritic syndrome (MCNS) were studied in order to clarify the characteristics of the immune system in MCNS and their relation to clinical activity. In the active phase (n = 17), serum immunoglobulin (Ig) M and E levels, B lymphocytes (surface Ig-positive cells) and their subsets, surface IgG, IgM and IgE positive cells; Bγ, Bμ and B∊, were increased, whereas the serum IgG level and OKT3-reactive cells, peripheral T lymphocytes; T3, were decreased. In the remitted phase maintained by steroid therapy (n = 17), serum Igs and and B lymphocytes subsets tended to return to normal levels concomitant with decreases in T3 and T4, and an increase in T8 in consequence of a marked decrease in T4/T8 (helper/suppressor) ratio. In stable remission continuing with no steroid therapy (n = 14), the above abnormalities returned to normal ranges, except for serum IgM which remained at a high level and re-elevated serum IgE. These results suggest that immunological abnormalities in MCNS are characterized by acceleration of the IgE and IgM producing systems and impaired maturation of the IgG producing system despite normal differentiation from the IgM producing to IgG producing system, possibly caused by T lymphocyte dysfunction. [ABSTRACT FROM AUTHOR]