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)

Using chromatographic technique on "Sephadex G 200" associated to immunologic qualitative and quantitative techniques, the authors showed that the alpha1-macroglobulin is present in normal Rat urines. This protein is also present in urines obtained during the Masugi nephritis. The alpha1-macroglobulin concentration observed in the different urine samples is unrelated to the total proteinuria evolution. The results given allow us to discuss the mechanisms of the glomerular filtration.
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PMID:[Changes in the level of alpha1-macroglobulin in rats during Masugi nephritis]. 5 Aug 89

The quantity of urinary proteins and their molecular weight composition was analyzed in different experimental glomerulopathies using the SDS-PAA-electrophoresis. Masugi nephritis, heterologous and autologous immune complex nephritis as well as D-penicillamine induced glomerulonephritis were studied in rabbits, guinea pigs and rats. The procedure allows (1) to distinguish physiological from low grade glomerular proteinuria by their respective characteristic patterns in early disease stages (2) to follow up the disease course of individual animals without sacrifice and (3) to discriminate species specificity of physiological urinary proteins. It is recommended to use this technique of urinary protein analysis in experimental conditions, where mild glomerular damage is expected.
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PMID:Molecular weight analysis of proteinuria in experimental glomerulopathies. 13 32

Structural distortion of glomerular capillaries in chronic rat Masugi nephritis was studied by light, transmission electron, and scanning electron microscopy. A few months after rats were given injections of heterologous nephrotoxic antibodies, focal and local mesangial as well as basement membrane thickenings were observed. Using scanning electron microscopy, glomerular corrosion castings disclosed that definite loop constriction with occasional gaps occurred in such local foci. The local changes were gradually extended to adjacent areas in rats with severe proteinuria, later resulting in a broad disappearance of the loops. Also observed were glomeruli undergoing a collapse with structural simplification resulting from multiple loss of communicating branches. At the terminal stage, almost all glomeruli were involved in varying degrees in either of these changes. In contrast, no progression of the disease process was observed in rats with minimal proteinuria. By scanning electron microscopy, a large number of castings from various angles revealed that morphologically normal glomeruli were involved in local and ultimately global obsolescence under the condition of persistent proteinuria.
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PMID:Structural distortion of glomerular capillary loops in the chronic phase of rat Masugi nephritis. 43 55

Pyridinol-carbamate (P.C.) is a new substance with various properties including an anti-inflammatory (anti-kinin) and an antiplatelet aggregation activity. Since a coagulation process has been demonstrated in Masugi nephritis in Rats, we investigated the effect of P.C. in this experimental model. P.C. (150 mg/kg/day) was given orally from day 1 to day 28. It prevented partially the G.N.: proteinuria was significantly lower than in nephritic untreated animals with a reduction of seromucoid blood levels and B.U.N. Histological examination revealed that glomerular injury was limited in treated animals specially with regards to G.B.M. alterations and deposits.
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PMID:[Action of pyridinol carbamate on hetero-immune Masugi nephritis in the rat (author's transl)]. 79 Feb 74

Participation of blood born cells in rat Masugi nephritis was investigated with ultrastructural demonstration of peroxidase, in addition to conventional light and electron microscopies. Polymorphonuclear leukocytes appear immediately and transiently after injection of nephrotoxic serum. Hypercellularity in the early stage of the disease is consisted mainly of monocyte-macrophage. Proteinuria and infiltration of few monocytes are persistent through the course up to 124 days and focal sclerosis with hyaline material appears in the later stage.
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PMID:Participation of blood born cells in rat Masugi nephritis. 98 5

The enzymatic activity of blood leukocytes was studied in rats with Masugi nephritis by means of the quantitative cytochemical method. Nephrotoxin injection during first hours and days did not produce specific changes in the enzymatic activity. Maximum changes were observed on the 8-th day when the elevation of the activity of dehydrogenase lymphocytes and neutrophils acid phosphatase was observed at the same time with most pronounced histological changes in the kidneys, the decrease of the complement titer and the presence of nephrotoxin and autoglobulin in the renal glomeruli. Later the histological changes became less pronounced, and the enzymatic activity decreased. In rats with proteinuria the activity of the neutrophil leukocytes acid phosphatase was higher than in animals without proteinuria.
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PMID:[Study of the enzymatic activity of the blood leukocytes in experimental nephrotoxic nephritis in rats]. 110 83

The effects of the reduction of neutrophils in glomeruli on the improvement of proteinuria and glomerular injuries were determined in the first (heterologous) phase of Masugi (nephrotoxic) nephritis. Male (6-week-old) WKA/Hkm rats were initially injected with 2.0 ml of a newly developed monoclonal antineutrophil antibody and then injected with 1.0 ml of nephrotoxins. This monoclonal anti-neutrophil antibody was found to have selectively reduced the number of neutrophils in the glomerular capillary lumen in cases of Masugi nephritis by light microscopy. Malondialdehyde (MDA) levels or superoxide dismutase (SOD) activities in renal tissues of such rats were also examined. However, there were no significant differences in the levels of proteinuria and the number of glomerular cells containing resident cells and infiltrated mononuclear cells in the first phase of Masugi nephritis with or without pretreatment with antineutrophil antibody. No significant differences were observed in the levels of MDA or SOD activities in renal tissues of Masugi nephritis with or without pretreatment with such an antibody either. It appeared that infiltration of neutrophils in the glomeruli might not be related to proteinuria and glomerular injuries in the first phase of Masugi nephritis. It was postulated that the massive proteinuria in the first phase of Masugi nephritis might be correlated with the activities of reactive oxygen species induced by the glomerular cells, i.e. glomerular resident cells and infiltrated mononuclear cells.
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PMID:Correlation between reduction of polymorphonuclear leucocytes in glomeruli injected with a newly developed monoclonal antineutrophil antibody and proteinuria in Masugi nephritis. 133 43

FK506 is a new drug which has potent immunosuppressive activity. We studied its immunosuppressive effects on active Heymann's nephritis and the autologous phase of Masugi nephritis. The induction of active Heymann's nephritis was completely suppressed by FK506 injected simultaneously with the antigen (day 1) and then daily for 14 days at a dose of 0.64 mg/kg per day or more. With a lower dosage of this agent, antibody production and immune deposits in the glomerular basement membrane occurred despite the suppression of proteinuria. Similar results were obtained in rats on other treatment schedules (1-7 days or day 8-14 days duration). Rats that were prevented from developing Heymann's nephritis or the autologous phase of nephrotoxic antiserum nephritis by FK506 treatment exhibited a suppressed immune response to a second immunization of the same antigen even 4 weeks after cessation of drug administration: however, they developed antibodies when inoculated with other antigens. Rat peripheral leucocyte counts and serum creatinin were not remarkably influenced by the administration of FK506. These results indicate that FK506 has potent immunosuppressive activity, and it is suggested that it is able to induce an antigen-specific immunotolerance.
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PMID:FK506, a novel immunosuppressive agent, induces antigen-specific immunotolerance in active Heymann's nephritis and in the autologous phase of Masugi nephritis. 170 73

Complement but not polymorphonuclear granulocytes (PMN) causes glomerular injury in passive Heymann nephritis in rats. We have now identified monocytes as another important mediator in this model. Passive Heymann nephritis was induced in Wistar rats by intravenous injection of sheep anti-rat Fx1A antiserum. Four groups (all receiving anti-rat Fx1A antiserum) were studied: (a) rats given normal sheep globulin (nephritic controls), (b) rats given sheep anti-rat PMN globulin (PMN-depleted), (c) rats given sheep anti-rat monocyte globulin (monocyte-depleted), (d) rats injected with cobra venom factor (complement-depleted). In vitro specificity controls for anti-cell antisera were made by cytotoxicity tests and inhibition of phagocytosis. In vivo specificity controls were performed in heterologous Masugi nephritis (PMN-dependent) and accelerated Masugi nephritis (monocyte-dependent). Complement and monocyte depletion significantly delayed the onset of proteinuria (p less than 0.001 versus nephritic controls on day 5), PMN depletion had no significant effect. Monocyte infiltration was seen in control nephritic rats, but monocyte depletion prevented this influx. In the monocyte-depleted group, no differences in glomerular deposition of C3, C9, and C5b-9 were seen in comparison to the nephritic control rats. Serum C3 levels were comparable in groups a, b, and c, the complement system was biologically active in the monocyte depleted-group (c), and the amount of anti-Fx1A antibody bound was the same in all groups. This shows that, besides complement, monocytes are required for induction of renal damage in passive Heymann nephritis. The concept of a sole role for complement in glomerular immune injury involving subepithelial immune deposits should be reconsidered.
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PMID:Complement and monocytes are essential for provoking glomerular injury in passive Heymann nephritis in rats. Terminal complement components are not the sole mediators of proteinuria. 157 58

1. Nephrotoxic serum nephritis was induced immunologically in uninephrectomized Sprague-Dawley rats (n = 24). One-half were assigned randomly to treatment with enalapril (5 mg/kg per 24 h). 2. Untreated rats (n = 12) developed a progressive fall in creatinine clearance, a progressive rise in systolic blood pressure and marked proteinuria over a 6 week period. The mortality rate was 42% at 5 weeks and 66% at 6 weeks. 3. Enalapril-treated rats (n = 12) had no significant reduction in systolic blood pressure, and a similar reduction in creatinine clearance to that in untreated rats. Mortality was 50% at 5 weeks, and 92% at 6 weeks. 4. Proteinuria but not the blood pressure rise was significantly reduced by enalapril treatment. 5. Converting enzyme inhibitors may have a specific role in the treatment of nephritic diseases.
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PMID:Effect of enalapril treatment on progression of the nephrotoxic serum nephritis model of renal failure in the rat. 285 51


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