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  • 1
    Electronic Resource
    Electronic Resource
    Effect of cyclosporine therapy on idiopathic membranous nephropathy presented with refractory nephrotic syndrome (2000)
    Springer
    Clinical and experimental nephrology 4 (2000), S. 81-85 
    Details
    ISSN: 1437-7799
    Keywords: Key words Membranous nephropathy ; Nephrotic syndrome ; Cyclosporine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background. Recent studies suggested the possible benefits of cyclosporine (CsA) therapy in patients with membranous nephropathy, although most of these studies were short-term. An uncontrolled retrospective study was undertaken to evaluate the long-term effect of CsA therapy on idiopathic membranous nephropathy presented with refractory nephrotic syndrome. Methods. The subjects were eight patients with idiopathic membranous nephropathy presenting with refractory nephrotic syndrome. All patients had received a course of corticosteroid therapy before CsA therapy, and had not responded to the corticosteroid, including one or two administrations of intravenous methylprednisolone pulse therapy. The CsA doses were adjusted to maintain trough blood level at 100 ng/ml during the first 3 months and then reduced to maintain the level at 50 ng/ml in patients who had responded to partial remission. Results. CsA therapy induced a marked decrease in proteinuria from the first month, and a significant decrease from month 3 and thereafter. The mean serum total protein and albumin levels rose, and total cholesterol fell significantly with CsA therapy. The serum creatinine level was unchanged during CsA therapy. Three patients showed complete remission and two were in partial remission, while three were nephrotic at 12 months of CsA therapy. From 18 to 24 months of CsA therapy, three patients were in complete remission, four were in partial remission, and one patient was nephrotic. There were no side effects of CsA, except for gum hyperplasia and hypertrichosis in one patient. Conclusion. These results suggest that long-term CsA therapy at a low or moderate dose is potentially effective and safe in most nephrotic patients with idiopathic membranous nephropathy refractory to corticosteroid therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s101570050068
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of anti-insulin antibody on insulin binding to liver membranes: evidence against antibody-induced enhancement of insulin binding to the insulin receptor (1986)
    Springer
    Diabetologia 29 (1986), S. 447-452 
    Details
    ISSN: 1432-0428
    Keywords: Anti-insulin antibody ; insulin receptor ; insulin binding ; cross-linking ; disuccinimidyl suberate ; Fcy receptor ; liver membrane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the presence of anti-insulin antibody, 2- to 3-fold enhancement of 125I-insulin binding to liver membranes was observed when binding was estimated by the radioactivity of 125I-insulin bound to the membrane pellets. However, after 125'I-insulin was covalently cross-linked to liver membranes using disuccinimidyl suberate in the presence of anti-insulin antibody, sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography showed that 125I-insulin bound to the α-subunit of the insulin receptor was inhibited by antiinsulin antibody in an dose-dependent manner. More importantly, at an anti-insulin antibody dilution range between 1:50 and 1:5,000, sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed two 125I-labelled bands of mol wt 62,000 and 27,000, while only one band of mol wt 130,000 was revealed in the absence of anti-insulin antibody. These Mr=62,000 and Mr=27,000 bands were found to be the heavy and the light chain of anti-insulin IgG molecules respectively. Pepsin digested anti-insulin serum had only an inhibitory effect on 125I-insulin binding to liver membranes. Non-immunized guinea pig serum or IgG completely abolished the enhanced effect of anti-insulin antibody. Further, this enhanced effect was inhibited by Fc fragment-specific anti-IgG serum or H&L-chain-specific anti-IgG serum in a dosedependent manner. Protein A also inhibited the effect of antiinsulin antibody. In IM-9 lymphocytes and human red blood cell ghosts, which have no Fcy receptors, enhancement of insulin binding was not observed in the presence of anti-insulin antibody. These data suggest that anti-insulin antibody-induced enhancement of insulin binding to liver membranes is not due to the enhanced binding to the insulin receptor itself but probably due to the binding of insulin-anti-insulin antibody complex to the Fcγ receptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00506537
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    Paper (German National Licenses)
    Fulltext
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