Mechanisms of progression in glomerulonephritis.
Although most forms of glomerulonephritis in man are thought to have an immunopathogenesis, certain clinical and experimental observations support the role of other non-immunologic mechanisms in the progression of these diseases. 1. Intra-renal vascular disease thought to be secondary to hypertension, may be responsible for ischemic glomerular sclerosis. 2. Hypertension may damage the diseased glomerulus directly, as has been demonstrated in experimental glomerulonephritis, in the remnant kidney, and in experimental diabetes mellitus. 3. Alterations in glomerular structure and function in the remnant kidney suggest that adaptations to nephron loss may contribute to further renal damage. 4. Glomerular sclerosis occurs under circumstances where immunologic mechanisms are highly unlikely, such as aging, reflex nephropathy, chronic aminonucleoside administration, and protein loading. 5. Preservation of renal function can be achieved by phosphorus restriction in the remnant kidney and in nephrotoxic serum nephritis.
D000818:Animals; D005921:Glomerulonephritis / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D005923:Glomerulosclerosis, Focal Segmental / Q000209:etiology; D006801:Humans; D006973:Hypertension / Q000150:complications; D007111:Immunity, Cellular; D007668:Kidney / Q000098:blood supply; D009404:Nephrotic Syndrome / Q000503:physiopathology; D010758:Phosphorus / Q000502:physiology; D051381:Rats
D010758:Phosphorus