Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of cyclosporin A on the development of the autologous phase of experimental rabbit glomerulonephritis was assessed. The glomerulonephritis was induced by an intravenous injection of duck anti-rabbit glomerular basement membrane globulin into adult rabbits. After 5-7 days, diffuse proliferative glomerulonephritis with proteinuria and linear glomerular basement membrane deposits of rabbit IgG were observed in all animals. The cyclosporin A treatment was started simultaneously with the injection of duck globulin. This attenuated the glomerular lesion, resulting in a normal urinary excretion. The serum level of anti-duck globulin antibody was reduced. In the group of rabbits, receiving an injection of duck anti-rabbit glomerular basement membrane globulin, cyclosporin A treatment and an additional high dose of rabbit anti-duck globulin 8 days later, equally no glomerulonephritis was observed. However, no effect of cyclosporin A treatment on the duck immunoglobulin induced passive Arthus phenomenon was seen.
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PMID:[The effect of cyclosporin A on experimental glomerulonephritis in rabbits]. 219 71

Experiments were designed to test the effect of a receptor antagonist of platelet activating factor (PAF), SRI63072, on inflammatory injury induced by in situ formation of immune complexes in two vascular districts of the rat that have different structural and hemodynamic characteristics: unilateral glomerulonephritis induced by perfusion of the left kidney of preimmunized animals with cationic human IgG, and passive reversed Arthus reaction in the skin. Three days after perfusion the left kidneys of rats not treated with SRI63072 (group I) were greatly enlarged, and pale and severe exudative and proliferative lesions were present in glomeruli. Granular deposits of human IgG, rat IgG, and rat C3 were seen by immunofluorescence microscopy, and subepithelial electron-dense deposits were visualized by electron microscopy. The right kidneys were consistently normal. The animals were severely proteinuric and had increased levels of PAF in the circulation. In contrast, rats treated with SRI63072 (group II) and studied at the same interval of time developed only mild, focal glomerulonephritis in the perfused kidneys. By immunofluorescence microscopy the glomerular deposits of human IgG and rat IgG were similar in quantity and distribution to those observed in rats of group I. Despite the fact that SRI63072 did not influence the level or the activity of the rat serum complement system, the deposits of C3 were less abundant and more focal. As in animals of group I, electron-dense deposits were present at the epithelial side of the glomerular basement membrane. Proteinuria was slight, and levels of circulating PAF were not significantly increased. These effects cannot be ascribed to interference of SRI63072 with antigen "implantation," antibody binding, or local hemodynamic conditions, because the amounts of glomerular human and rat IgG were the same in treated and untreated rats; SRI63072 did not decrease the glomerular filtration rate; and SRI63072 prevented the increase in vascular permeability and the exudative lesions in passive Arthus reaction in the skin, a model less affected by hemodynamic changes than glomerulonephritis. The beneficial effect of SRI63072 indicates that PAF is an important mediator of the inflammatory process generated either in glomeruli or in the skin by in situ immune complex formation.
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PMID:Receptor antagonist of platelet activating factor inhibits inflammatory injury induced by in situ formation of immune complexes in renal glomeruli and in the skin. 295 66

The effect of cyclosporin A on the development of the autologous phase of experimental rabbit glomerulonephritis was assessed. The glomerulonephritis was induced by a single intravenous injection of duck anti-rabbit glomerular basement membrane globulin (molecular weight: 115 kDa) into adult rabbits. After 5-7 days, diffuse proliferative glomerulonephritis with proteinuria was observed in all the animals not treated with cyclosporin A (control group). The cyclosporin A treatment was started simultaneously with the injection of duck globulin. This attenuated the glomerular lesion, resulting in a normal urinary protein excretion. The serum level of autologous anti-duck IgG was reduced. In the group of rabbits which received an injection of duck anti-rabbit glomerular basement membrane globulin, cyclosporin A treatment and an additional high dose rabbit anti-duck globulin 8 days later again no glomerulonephritis was observed. However, cyclosporin A treatment had no effect on the observed duck immunoglobulin-induced passive Arthus phenomenon.
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PMID:The effect of cyclosporin A on rabbit nephrotoxic glomerulonephritis. 847 35

Induction of immunotolerance was studied in the autologous phase of experimental rabbit glomerulonephritis. The glomerulonephritis was induced by intravenous injection of duck anti-rabbit glomerular basement membrane globulin into rabbits. One single intravenous injection of that nephrotoxis immunoglobulin (20 mg/kg body weight) into rabbits was followed by glomerulonephritis with glomerular hypercellularity and proteinuria. Another group of rabbits was pretreated on their first day of age, using 1.5 mg/animal of immunoglobulin from duck. Nephritis did not grow manifest when the animals received another injection (20 mg/kg body weight), after eight weeks. Passive (intracutaneous) Arthus reaction (triggered by duck immunoglobulin) was recordable with equal intensity from either group.
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PMID:[Immune tolerance in Masugi nephritis]. 849 18