MONONUCLEAR CELL SUBSETS IN IGM MESANGIAL PROLIFERATIVE GLOMERULONEPHRITIS - A COMPARATIVE-STUDY WITH MINIMAL CHANGE NEPHROTIC SYNDROME ANDIMMUNONEGATIVE MESANGIAL PROLIFERATIVE GLOMERULONEPHRITIS

Glomerular and interstitial leukocyte subpopulations were analyze in r enal biopsies from 18 patients with IgM mesangial proliferative glomer ulonephritis (IgM MPGN), 19 patients with minimal change nephrotic syn drome (MC) and 10 patients with immune-negative mesangial proliferativ e glomerulonephritis (IN MPGN), by immunoperoxidase techniques with mo noclonal antibodies. Mesangial cell proliferation was strongly correla ted with absolute numbers of intraglomerular T lymphocytes (r = 0.71; p < 0.01) in IgM MPGN, but not in MC or IN MPGN. Significant differenc es were found in the numbers of macrophages, CD4- and CD8-positive glo merular 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 < 0.0 1, 0.05 and 0.05, respectively), the greatest and smallest values appe aring in IgM MPGN and MC, respectively. Multiple regression test showe d initial proteinuria values in IgM MPGN to be closely dependent on th e density of neutrophils, macrophages, T and B lymphocytes and CD4 cel l inflammatory infiltrates (r2 = 0.92; p < 0.01). At the end of the fo llow-up, proteinuria in IgM MPGN, but not in MC or IN MPGN, was depend ent on T cell infiltrate (r2=0.97; p<0.01). Our findings suggest that proteinuria in IgM MPGN results from local mesangial damage rather tha n from the effects of a soluble circulating factor, as has been propos ed for MC. The clinical and immunohistochemical differences observed b etween these two processes support the notion that they should be cons idered as separate entities.