Cell mediated immunity in idiopathic glomerulonephritis.

Various recent reports have suggested the presence of a functional defect of lymphocyte subpopulations in minimal-change nephropathy during the active phase. A probable role of inhibitory humoral factor(s) has been hypothesized. However, other authors have been unable to detect a significant difference between plasma from patients with nephrotic syndrome due to minimal-change nephropathy and plasma from other glomerulonephritis in the degree of inhibition of mitogen-induced lymphocyte transformation. In our study, T cell function, as measured by the response to PHA in autologous plasma, was depressed only in patients with minimal-change nephrotic syndrome and in patients with membranoproliferative glomerulonephritis. The lymphocyte function returned to normal when lymphocytes were cultured in homologous plasma. The lymphocyte responsiveness of patients with other glomerulonephritis with or without nephrotic syndrome was normal in both autologous and homologous plasma. Moreover, only plasma from patients with minimal-change nephropathy in the active phase and with membranoproliferative glomerulonephritis were able to induce inhibition of mitogenesis of lymphocytes from healthy donors. These data seem to confirm the presence of specific humoral inhibitory factor(s) in the plasma of these patients. Finally, preliminary findings seem to demonstrate an increase of the number of TG cells in patients with minimal-change nephropathy in remission who relapse early in the subsequent follow-up.