Glomerular monocyte infiltration was evaluated by histochemical means (nonspecific esterase) and/or electron microscopy in 305 renal biopsies belonging to a wide variety of human renal diseases. Significant monocyte infiltration was never observed in a first group of nepropathies (minimal change disease, nephrotic syndrome with IgM deposits, focal segmental glomerulosclerosis, membranous GN, Berger's GN, healed GN, dense deposit disease, chronic non specific GN, benign familial haematuria, Alport's disease, renal amyloidosis, arteriosclerotic kidney, light chain GN). Conversely, it was present at varying frequency in a second group of nephropathies including: acute GN (58.3%), persistent GN (10%), membranoproliferative GN (25.2%), eryoglobulinaemic GN (82.6%), lupus GN (36%), extracapillary proliferative GN (50%) and Schoenlein-Henoch GN (40%). The results indicate: 1) there is an evident association between monocyte infiltration and the subendothelial site of deposits; 2) the presence of monocytes is not affected by the size and extension of subendothelial deposits; 3) monocytes were more frequently observed when IgG, IgM and fibrinogen were present in the subendothelial deposits, Conversely, complement fractions do not seem to affect monocytic activity; 4) polymorphonuclear leukocyte exudation is less frequently found and mostly associated with monocyte infiltration; 5) in some GNs (persistent GN, cryoglobulinaemic GN and membranoproliferative GN), proteinuria was significantly higher in patients with than in those without monocyte infiltration, giving support to the hypothesis that in human beings as in experimental animals monocytes play a role in the pathogenesis of proteinuria.
Glomerular monocyte infiltration in human nephropathies: prevalence and correlation with clinical and morphological variables.
MAZZUCCO, Gianna;
1985-01-01
Abstract
Glomerular monocyte infiltration was evaluated by histochemical means (nonspecific esterase) and/or electron microscopy in 305 renal biopsies belonging to a wide variety of human renal diseases. Significant monocyte infiltration was never observed in a first group of nepropathies (minimal change disease, nephrotic syndrome with IgM deposits, focal segmental glomerulosclerosis, membranous GN, Berger's GN, healed GN, dense deposit disease, chronic non specific GN, benign familial haematuria, Alport's disease, renal amyloidosis, arteriosclerotic kidney, light chain GN). Conversely, it was present at varying frequency in a second group of nephropathies including: acute GN (58.3%), persistent GN (10%), membranoproliferative GN (25.2%), eryoglobulinaemic GN (82.6%), lupus GN (36%), extracapillary proliferative GN (50%) and Schoenlein-Henoch GN (40%). The results indicate: 1) there is an evident association between monocyte infiltration and the subendothelial site of deposits; 2) the presence of monocytes is not affected by the size and extension of subendothelial deposits; 3) monocytes were more frequently observed when IgG, IgM and fibrinogen were present in the subendothelial deposits, Conversely, complement fractions do not seem to affect monocytic activity; 4) polymorphonuclear leukocyte exudation is less frequently found and mostly associated with monocyte infiltration; 5) in some GNs (persistent GN, cryoglobulinaemic GN and membranoproliferative GN), proteinuria was significantly higher in patients with than in those without monocyte infiltration, giving support to the hypothesis that in human beings as in experimental animals monocytes play a role in the pathogenesis of proteinuria.
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