Monoclonal antibody analysis of glomerular hypercellularity in human glomerulonephritis.

To determine the contribution of infiltrating circulating leucocytes to glomerular hypercellularity, and to further investigate the immune and inflammatory mechanisms involved in human glomerulonephritis, a series of renal biopsies were evaluated using cell-specific monoclonal antibodies. In ninety-three renal biopsies from patients with glomerulonephritis, intraglomerular leucocytes were identified by immunoperoxidase localization of monoclonal antibodies to the leucocyte-common antigen, and antigens characteristic of T-cell and T-cell subsets, B-cells, monocytes and granulocytes. Normal glomeruli contained a mean of 2 leucocytes, predominantly monocytes, per glomerular cross-section. No significant increase in leucocytes was found in 41 biopsies with non-proliferative types of glomerulonephritis. However, in renal biopsies from 22 of the 46 patients with proliferative forms of glomerulonephritis, there was a significant increase in glomerular leucocytes. These biopsies were from 5 patients with post-infectious glomerulonephritis (mean of 30 leucocytes per glomerulus), 11 patients with crescentic glomerulonephritis (mean of 16 leucocytes per glomerulus) and 6 patients with mesangial proliferative glomerulonephritis due to systemic lupus erythematosus (mean of 5 leucocytes per glomerulus). The increased intraglomerular leucocytes consisted of macrophages and granulocytes. T and B-cells were generally not found within glomeruli. Thus, glomerular hypercellularity in proliferative glomerulonephritis is in part due to infiltration by inflammatory cells. No evidence was found to directly incriminate cellular immune mechanisms in the pathogenesis of the glomerular lesions of glomerulonephritis since T-cells were not identified within glomeruli.