Abstract
Immunological mechanisms play an important part in the pathogenesis of most human glomerular disease. Damage to glomeruli may result either from the deposition of immune complexes along the glomerular basement membrane (GBM) or from the fixation of specific anti-GBM antibodies to the GBM. These two mechanisms are usually readily distinguished by direct immunofluorescence tests which reveal the pattern of distribution of immune reactants within the diseased kidney. Immune complex deposits have a characteristic discrete, granular appearance which can be detected by staining with fluorescein-labeled antibodies to immunoglobulins, complement, or the relevant antigen. In contrast, binding of anti-GBM antibody is recognized by a continuous, finely linear staining pattern. It is now well established that the tubules and interstitium of the kidney are also susceptible to injury initiated by the deposition of immune complexes or antibodies to the tubular basement membrane (TBM) (1, 2, 3). Interstitial inflammation and abnormalities of the tubular epithelium and the TBM may result when immunoglobulin G (IgG), with or without complement (C), is present in granular or linear deposits in renal tubules and interstitium.
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Noble, B., Andres, G.A. (1981). Immunologically Mediated Tubular and Interstitial Nephritis. In: Strauss, J. (eds) Pediatric Nephrology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-8804-3_12
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DOI: https://doi.org/10.1007/978-1-4684-8804-3_12
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