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Non-complement-fixing immune complexes were detected by EA rosette inhibition in the sera of 47% of patients with primary glomerulonephritis (GN) and 60% with GN associated with systemic disease. Fifteen patients with minimal-change nephrotic syndrome (MCNS) in relapse produced significantly greater inhibition than the sera from 11 who were in remission. [ABSTRACT FROM AUTHOR]

We have confirmed our previous observation that improved human renal allograft survival is associated with the presence in pre-transplant serum of a high molecular weight lymphocyte Fcγ receptor-blocking factor. Scrum fractionation studies suggest that this factor is a complex protein consisting of IgG together with an IgG-binding protein which has an apparent molecular weight of approximately 60 kD. [ABSTRACT FROM AUTHOR]

The effect of blood transfusion on humoral immunity in chronic renal failure was studied by examining immunoglobulin production in vitro, in patients awaiting renal transplantation. Pokeweed mitogen (PWM) induced IgG plaque formation was normal in non-transfused uraemic patients while both spontaneous and Staphylococcus aureus Cowan I (SAC) induced immunoglobulin production were reduced. Five to ten units of third party blood transfusion reduced PWM-driven B cell differentiation, but had no effect on SAC-induced plaque formation, while spontaneous production of immunoglobulin was either enhanced or unaffected. As it is known that the response to SAC is less affected by suppressor T cell activity than that to PWM, these differences in the inhibitory effects of blood transfusion on B cell differentiation are further evidence that transfusion may act by increasing suppressor T cell activity. [ABSTRACT FROM AUTHOR]

We have investigated the immune responses in vitro of uraemic patients undergoing regular haemodialysis or continuous ambulatory peritoneal dialysis. Twenty-five healthy subjects were also studied as controls. In uraemic patients, the number of T and B lymphocytes were within the normal range, but proliferative respones to phytohaemagglutinin (PHA) were impaired. Spontaneous immunoglobulin plaque forming cell (PFC) responses by peripheral blood mononuclear cells (PBMC) from uraemic patients were significantly lower than those of healthy subjects. The PFC response of uraemic PBMC to the T cell independent polyclonal B cell activator (PBA) Epstein-Barr virus (EBV) was comparable to the response of the healthy subjects, indicating that uraemic B cells are still capable of synthesizing immunoglobulin. Pokeweed mitogen (PWM) induced PFC responses of uraemic PBMC were also normal, whereas the response to another T cell dependent B cell activator, Staphylococcus aureus Cowan I (SAC), was very low. Addition of indomethacin to PWM- and SAC-activated cultures of uraemic PBMC enhanced the PFC response to SAC, but had little effect on the PWM response. As full differentiation of B cells in response to SAC depends on helper T cells, we conclude that a defect in T lymphocyte function accounts for the reduced spontaneous and SAC induced production of immunoglobulin by uraemic PBMC. This defect may be mediated by an indomethacin-sensitive mechanism. [ABSTRACT FROM AUTHOR]