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)

NZB/NZW F1 female mice were treated with the immunosuppresive enzyme L-asparaginar antibodies, diminished deposition of gamma-globulins in kidneys, significantly delayed the onset of proteinuria, and reduced deaths from nephritis. These effects were associated with reduction of cellular IgM antibody synthesis to both T-dependent and T-independent antigens, but the graft-versus-host reaction was not affected. After several weeks of therapy, antibodies against Asnase appeared in the circulation, the effect on antibody synthesis was lost, ANA and anti-DNA appeared, followed by proteinuria and deaths from nephritis. Therefore Asnase proved to be an effective therapy in NZB/NZW mice, but its usefulness was limited by the appearance of inactivating antibodies.
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PMID:Effect of altered lymphocyte function on immunologic disorders in NZB/NZW mice. 1 1

In experiments on two groups of mongrel rats (4 weeks old and 4 months old) with induced nephrotoxic nephritis it was revealed that in comparison with adult rats the course of nephritis in ratlings was characterized by lesser proteinuria, selective in nature, by lesser reducticn of endogenous creatinine clearance and diuresis. The acido- and ammo-niogenesis decreased in ratlings and adult rats to the same extent. Morphological changes in the kidneys of ratlings were less pronounced than in adult animals, and were mostly localized in the convoluted tubules. The level of DNA-synthetic activity of the epithelial nuclei of the glomeruli prevailed over this index of the convoluted tubules epithelium. The weight index of the kidneys increased less in ratlings with nephritis than in adult rats. beta-lipoproteinemia in ratlings increased 8 times. Normalization of the urine and blood indices occurred more rapidly in ratlings than in adult rats.
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PMID:[Age and the course of nephrotoxic nephritis in rats]. 3 56

NZB/W F1 female mice were treated from 20 weeks of age with ribavirin (a broad spectrum antiviral drug), cyclophosphamide, or saline. Treatment with ribavirin (250 mg/kg twice weekly) prolonged survival from 9.8 to 18.5 months, reduced anti-DNA antibodies, and prevented proteinuria. Ability of ribavirin to prolong survival was dose related when given on a twice weekly schedule. However, daily ribavirin (25 mg/kg/day) was as effective as higher intermittent doses. Optimal ribavirin therapy was equal to cyclophosphamide treatment with regard to prolongation of survival. Ribavirin treatment did not significantly alter the body weight, hematocrit, WBC count, serum immunoglobulins, or Coombs reactivity. No alterations in either cellular or humoral immune responses were noted in NZB/W F1 or BALB/c mice treated for prolonged periods with ribavirin. The impressive therapeutic response to a broad spectrum antiviral agent seen in mice already manifesting immune complex nephritis provides a new therapeutic approach to the treatment of autoimmunity.
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PMID:Ribavirin treatment in murine autoimmune disease. I. Therapeutic efficacy and effect on the immune response. 3 80

Extracorporeal immunoadsorption and filtration was used in treatment of a 29-year-old woman with severe lupus nephritis. For the previous 35 days single-stranded DNA (ssDNA) antibody and immune-complex levels had been continuously raised with only partial improvement on prednisone therapy. Levels of immune complexes and ssDNA antibodies were substantially reduced by extracorporeal plasma filtration and adsorption of DNA collodion charcoal. There were no major clinical complications. After perfusion, the reduction of ssDNA binding and immune complexes in serum was sustained, serum C'3 became normal, and serum creatinine and proteinuria improved. 28 days after perfusion, subendothelial glomerular deposits were much reduced compared with those in a pre-perfusion biopsy specimen. Selective immunoadsorption is a promising new approach to persistent lupus nephritis refractory to drug therapy alone.
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PMID:Extracorporeal immunoadsorption: initial experience in human systemic lupus erythematosus. 9 Sep 20

Pharmacologic quantities of prostaglandin alter the immune complex nephritis of NZB/W mice. To study the mechanism of this change, NZB/W mice received 200 micrograms. of prostaglandin E1 or E2 twice daily starting at 2, 4, or 6 months of age. Mice were sacrificed at bimonthy intervals, renal function and serologic parameters were evaluated, and renal tissue was examined by light, fluorescence, and electron microscopy. Therapy decreased the incidence of proteinuria, lessened renal pathology, and prolonged survival. Maximal beneficial effects occurred when treatment began at 2 months of age. The most striking change was a decrease in the rate of immune complexes depositing in the mesangium and their absence from peripheral loops. Accompanying this change was a reduction in glomerular hypercellularity and a decrease in renal perivascular and interstitial mononuclear infiltrates. By contrast, treatment did not alter serum levels of immunoglobulins, antinuclear antibodies, and antisingle or double-stranded DNA. These results indicate that prostaglandin E is capable of prolonging survival in NZB/W mice by decreasing the rate of immune complexes depositing in glomeruli.
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PMID:Effect of prostaglandin E on immune complex nephritis in NZB/W mice. 15 78

Ribavirin, a drug with known antiviral activity, was given to mice with established lupus nephritis. Ribavirin was effective in prolonging survival, reducing the titer of antibodies to DNA, and reversing proteinuria. Other antiviral agents were not effective in the dosages used.
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PMID:Ribavirin: efficacy in the treatment of murine autoimmune disease. 29 57

Adult female (NZB + NZW)F1 mice were treated with cortisone, cortisone with tolerogen (isologous NZB IgG-nucleosides conjugates) or cortisone with isologous IgG free of nucleosides. Other treatments also included tolerogen or isologous IgG alone, and cortisone together with denatured DNA. All untreated mice died by 10 mo of age. Cortisone prolonged the survival rate. This effect was further improved by combined treatment of cortisone and tolerogen. Prolonged survival was accompanied by a decrease in proteinuria. Other treatments failed to influence either survival or proteinuria. Although cortisone did not prevent the appearance of antibody to denatured DNA, cortisone and tolerogen suppressed them in most of the animals. Preexisting antibody to denatured DNA was reduced by cortisone and cortisone and tolerogen, but not by cortisone and IgG. In contrast, antibody to native DNA bore no relationship to therapy. Animals living beyond 1 yr of age, regardless of the treatment, fall into three histopathological categories: (a) severe nephritis, as in untreated animals, (b) moderate nephritis (with absence of severe alteration of the glomerular basement membrane, i.e. the histological counterpart of prolonged survival), (c) minimal nephritis. In a small number of animals treated with cortisone or cortisone and IgG and in 6/20 animals treated with cortisone and tolerogen, minimal lesions as judged by light, fluorescent, and electron microscopy were found. These last mice were in good health at 15-16 mo of age, twice the life-span of untreated mice. In conclusion, these data suggest that tolerance to nucleic acid antigens facilitated by cortisone offers a promising new approach to treat established murine lupus nephritis.
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PMID:Treatment of lupus nephritis in adult (NZB + NZW)F1 mice by cortisone-facilitated tolerance to nucleic acid antigens. 30 53

Administration of thymosin fraction V to NZB/NZW F1 mice, an animal model for human SLE, accelerated the appearance of proteinuria and anti-nDNA antibodies, increased deposition of immunoglobulins in kidneys, and significantly shortened survivals. Although the addition of thymosin to in vitro cultures of spleen and lymph node cells from thymosin-treated mice increased DNA synthesis in response to stimulation with Con A, in vivo treatment with thymosin did not affect the Con A response. There was no effect on in vitro responses to PHA or LPS, or on IgM antibody formation to SRBC (T cell dependent) or SSS III (T cell independent) immunizations. Antibodies to thymosin or contamination of our thymosin preparations with nucleic acids could not be demonstrated. The acceleration of autoimmune disease produced by thymosin treatment could not be explained by alteration of the T and B cell functions studied.
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PMID:Effect of altered lymphocyte function on immunologic disorders in NZB/NZW mice. III. Acceleration of disease by thymosin. 30 81

Treatment of female NZB/W F1 mice with Nafoxidine, an anti-estrogen, led to delayed manifestation of autoimmune features. Such treated mice had reduced anti-DNA antibodies, reduced proteinuria, and improved survival. These results support the hypothesis that sex hormones play an important role in the expression of autoimmunity and suggest that estrogens may accelerate autoimmunity in NZB/W F1 mice.
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PMID:Effect of the anti-estrogen, Nafoxidine, on NZB/W autoimmune disease. 30 24

NZB/NZW mice spontaneously exhibit autoimmune disease similar to that seen in human systemic lupus erythematosus (SLE). We demonstrated that total lymphoid irradiation (TLI) reversed well expressed disease in 6-mo-old NZB/NZW females with a prolongation in survival, decrease in proteinuria, and decrease in anti-DNA antibodies as compared to control animals. Few side effects were observed in the treated group. TLI also prolonged survival in animals with advanced renal disease. These findings suggest that TLI may have application to the treatment of human SLE.
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PMID:Reversal of nzb/nzw disease with total lymphoid irradiation. 31 31


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