Mononuclear cell subsets in IgM mesangial proliferative glomerulonephritis. A comparative study with minimal change nephrotic syndrome and immunonegative mesangial proliferative glomerulonephritis.

Glomerular and interstitial leukocyte subpopulations were analyzed in renal biopsies from 18 patients with IgM mesangial proliferative glomerulonephritis (IgM MPGN), 19 patients with minimal change nephrotic syndrome (MC) and 10 patients with immune-negative mesangial proliferative glomerulonephritis (IN MPGN), by immunoperoxidase techniques with monoclonal antibodies. Mesangial cell proliferation was strongly correlated with absolute numbers of intraglomerular T lymphocytes (r = 0.71; p < 0.01) in IgM MPGN, but not in MC or IN MPGN. Significant differences were found in the numbers of macrophages, CD4- and CD8-positive glomerular cells (Student's t test p < 0.01, 0.05 and 0.01, respectively) in IgM MPGN, but not in MC or IN MPGN. The numbers of CD45-, CD3- and CD8-positive cells also differed in each patient group (ANOVA p < 0.01, 0.05 and 0.05, respectively), the greatest and smallest values appearing in IgM MPGN and MC, respectively. Multiple regression test showed initial proteinuria values in IgM MPGN to be closely dependent on the density of neutrophils, macrophages, T and B lymphocytes and CD4 cell inflammatory infiltrates (r2 = 0.92; p < 0.01). At the end of the follow-up, proteinuria in IgM MPGN, but not in MC or IN MPGN, was dependent on T cell infiltrate (r2 = 0.97; p < 0.01). Our findings suggest that proteinuria in IgM MPGN results from local mesangial damage rather than from the effects of a soluble circulating factor, as has been proposed for MC. The clinical and immunohistochemical differences observed between these two processes support the notion that they should be considered as separate entities.