Abstract
The increasing use of percutaneous renal biopsy techniques, together with the recent application of electron and immunofluorescent microscopy to these biopsies, has enabled the demarcation of primary glomerular diseases as one of the important large group of parenchymal renal diseases. In these primary glomerular diseases, the pathological changes appear to originate in, and predominantly to affect the glomeruli, although there may be concomitant changes in other parts of the kidney, and the renal changes may be part of a generalized process occurring elsewhere in the body. Included under primary glomerular diseases are the diffuse processes of acute proliferative and exudative glomerulonephritis, membranous glomerular disease, mixed membranous and proliferative glomerulonephritis, lipoid nephrosis and toxaemia of pregnancy, and the focal glomerular diseases. The salient morphological features of acute diffuse glomerulonephritis include intracapillary cell proliferation and exudation, in varying proportions, together with the presence of characteristic electron thickening of the capillary walls due to widespread subepithelial deposits. It is of great clinical importance to distinguish membranous glomerular disease from lipoid nephrosis, in which widespread fusion of epithelial foot processes, in the absence of other significant changes, is the diagnostic feature. Mixed membranous and proliferative glomerulonephritis involves variable hypercellularity in different capillary loops, together with thickening of some but not all peripheral capillary walls. The renal changes seen in toxaemia of pregnancy include swelling of endothelial cells together with irregular thickening of the lamina rara interna of the capillary basement membrane. Focal glomerular disease is a relatively common finding in most large series of renal biopsies. A small proportion of these cases are associated with systemic lupus nephropathy, Henoch-Schonlein purpura, so-called Goodpasture's syndrome, and subacute bacterial endocarditis, but in the vast majority we have no idea of the aetiology of the focal glomerular lesions. The increasing use of percutaneous renal biopsy techniques, together with the recent application of electron and immunofluorescent microscopy to these biopsies, has enabled the demarcation of primary glomerular diseases as one of the important large group of parenchymal renal diseases. In these primary glomerular diseases, the pathological changes appear to originate in, and predominantly to affect the glomeruli, although there may be concomitant changes in other parts of the kidney, and the renal changes may be part of a generalized process occurring elsewhere in the body. Included under primary glomerular diseases are the diffuse processes of acute proliferative and exudative glomerulonephritis, membranous glomerular disease, mixed membranous and proliferative glomerulonephritis, lipoid nephrosis and toxaemia of pregnancy, and the focal glomerular diseases. The salient morphological features of acute diffuse glomerulonephritis include intracapillary cell proliferation and exudation, in varying proportions, together with the presence of characteristic electron thickening of the capillary walls due to widespread subepithelial deposits. It is of great clinical importance to distinguish membranous glomerular disease from lipoid nephrosis, in which widespread fusion of epithelial foot processes, in the absence of other significant changes, is the diagnostic feature. Mixed membranous and proliferative glomerulonephritis involves variable hypercellularity in different capillary loops, together with thickening of some but not all peripheral capillary walls. The renal changes seen in toxaemia of pregnancy include swelling of endothelial cells together with irregular thickening of the lamina rara interna of the capillary basement membrane. Focal glomerular disease is a relatively common finding in most large series of renal biopsies. A small proportion of these cases are associated with systemic lupus nephropathy, Henoch-Schonlein purpura, so-called Goodpasture's syndrome, and subacute bacterial endocarditis, but in the vast majority we have no idea of the aetiology of the focal glomerular lesions.
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