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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 69 (1991), S. 536-551 
    ISSN: 1432-1440
    Keywords: Vasculitis ; Polyarteritis ; Wegener's granuloma ; Anti-neutrophil Cytoplasmic antibody (ANCA) ; Schonlein-Henoch purpura ; Glomerulonephritis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary After a long period during which few new data on the vasculitides emerged, the past decade has seen a real explosion of data on the subject. This began with basic clinical descriptions and the deliniation of long term outcome as survival improved to a major extent under the influence of improved treatment regimes. In parallel, better understanding of the immunopathology has emerged. Of particular interest have been descriptions of autoantibody systems in vasculitis which seem to be specific to vasculitis and therefore diagnostically useful: the antineutrophil cytoplasmic antibodies (ANCA). Whether or not these are pathogenetically significant as well as useful remains a matter for debate. In parallel, anti endothelial cell antibodies have been described, but their role (if any), in pathogenesis remains equally obscure. There are some suggestions that vasculitis is becoming more common, but increased awareness and the availability of ANCA have undoubtedly increased awareness of the subject.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pediatric nephrology 6 (1992), S. 292-303 
    ISSN: 1432-198X
    Keywords: Glomerulonephritis ; Progression ; Tubulointerstitial changes ; Transforming growth factor β ; Adhesion molecules ; T lymphocytes ; Monocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract All recent studies of the outcome of different forms of progressive glomerulonephritis concur that a major factor, apparently determining outcome, is the presence and severity of tubulointerstitial changes, and not the degree of glomerular alteration. Moreover, at the time of biopsy, tubulointerstitial changes correlate much better with the glomerular filtration rate. These at first surprising findings are not only useful clinically, but should make us think about our models of how progression takes place in so-called glomerular nephritides. In fact, a major tubulointerstitial infiltrate of immune-competent cells is present in all forms of progressive glomerulonephritis, and again correlates with outcome. In addition, it is now clear the tubular epithelium is capable of synthesising and secreting a number of factors important in fibrogenesis, and of displaying major histocompatibility complex class II antigens and leucocyte-adhesion molecules. Tubular cells could thus present peptides to T helper cells and amplify, or maybe even initiate, immune reactions. Finally, fibrogenesis within the kidney is at last being studied, long after studies have been performed on liver and lung. In the past, too much attention has been paid to reversible inflammation and not enough to irreversible cirrhosis of the kidney.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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