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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review

Anti-Glomerular Basement Membrane Disease

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Disease relevance of Anti-Glomerular Basement Membrane Disease


High impact information on Anti-Glomerular Basement Membrane Disease


Chemical compound and disease context of Anti-Glomerular Basement Membrane Disease

  • The CI:G ratio was then used to determine whether mRNA measurements performed at an early stage of inflammation (day 7) in a model of anti-GBM disease in the rabbit would predict outcome at day 30 as measured by interstitial and glomerular scarring and renal cortical hydroxyproline accumulation [9].
  • RESULTS: Pretreatment with CyPh prevented glomerular leukocyte accumulation and completely inhibited proteinuria, glomerular cell proliferation and hypercellularity in accelerated anti-GBM disease [10].
  • Mice rendered completely deficient of the complement components C3 or C4 were used to determine the influence of complement activation in the heterologous phase of the anti-GBM disease model [11].
  • Factors affecting the glomerular protein leak after polyclonal activation in the HgCl2-induced model of anti-GBM disease in the brown Norway rat [12].
  • We also present data on 15 patients presenting to Guy's Hospital over the past 10 years with anti-GBM disease and creatinine > 500 mumol/l. The median delay from presentation to diagnosis was 7 days, range 1-81 days [13].

Biological context of Anti-Glomerular Basement Membrane Disease


Anatomical context of Anti-Glomerular Basement Membrane Disease


Gene context of Anti-Glomerular Basement Membrane Disease

  • To examine the genetic basis of susceptibility to anti-GBM disease in more detail, the HLA-DRB and DQB alleles inherited by 82 patients were analyzed using sequence specific oligonucleotides [19].
  • This identified a hierachy of association of DRB1 genes with anti-GBM disease, including susceptibility (DRB1*15, DRB1*04), neutral (DRB1*03) and protective (DRB1*07) alleles [19].
  • There was a significant increase in tubular p38 activation at 3 hours of anti-GBM disease, followed by increased JNK activation of the 54 kD isoform from day 7 onward, and the 46 kD isoform at day 28 [3].
  • The purpose of the present study therefore was to examine the role of heparanase in a model of accelerated anti-glomerular basement disease (anti-GBM) [20].
  • In the current study we used immunogold ultrastructural techniques to identify the exact sites of expression of ICAM-1 (CD54) in the glomerulus and the expression of CD11a and CD18 by infiltrating glomerular leukocytes in the first 24 hours of accelerated anti-GBM disease in rats [21].

Analytical, diagnostic and therapeutic context of Anti-Glomerular Basement Membrane Disease

  • On Western blotting, P1 bound to the same 6 bands in solubilized GBM (between 26 and 58 kilodaltons with major bands at 26 and 54 kilodaltons) that were recognized by sera from all 42 patients studied with anti-GBM disease [22].


  1. Blockade of p38alpha MAPK ameliorates acute inflammatory renal injury in rat anti-GBM glomerulonephritis. Stambe, C., Atkins, R.C., Tesch, G.H., Kapoun, A.M., Hill, P.A., Schreiner, G.F., Nikolic-Paterson, D.J. J. Am. Soc. Nephrol. (2003) [Pubmed]
  2. Hyaluronan-induced cyclooxygenase-2 expression promotes thromboxane A2 production by renal cells. Sun, L.K., Beck-Schimmer, B., Oertli, B., Wüthrich, R.P. Kidney Int. (2001) [Pubmed]
  3. Activation and cellular localization of the p38 and JNK MAPK pathways in rat crescentic glomerulonephritis. Stambe, C., Atkins, R.C., Hill, P.A., Nikolic-Paterson, D.J. Kidney Int. (2003) [Pubmed]
  4. Local macrophage proliferation in the pathogenesis of glomerular crescent formation in rat anti-glomerular basement membrane (GBM) glomerulonephritis. Lan, H.Y., Nikolic-Paterson, D.J., Mu, W., Atkins, R.C. Clin. Exp. Immunol. (1997) [Pubmed]
  5. Autoantibodies to myeloperoxidase aggravate mild anti-glomerular-basement-membrane-mediated glomerular injury in the rat. Heeringa, P., Brouwer, E., Klok, P.A., Huitema, M.G., van den Born, J., Weening, J.J., Kallenberg, C.G. Am. J. Pathol. (1996) [Pubmed]
  6. Fibronectin is the major fibroblast chemoattractant in rabbit anti-glomerular basement membrane disease. Gharaee-Kermani, M., Wiggins, R., Wolber, F., Goyal, M., Phan, S.H. Am. J. Pathol. (1996) [Pubmed]
  7. Antineutrophil-cytoplasmic antibodies and antiglomerular basement membrane antibodies in Goodpasture's syndrome and in Wegener's granulomatosis. Weber, M.F., Andrassy, K., Pullig, O., Koderisch, J., Netzer, K. J. Am. Soc. Nephrol. (1992) [Pubmed]
  8. The lipopolysaccharide-triggered mesangial transcriptome: Evaluating the role of interferon regulatory factor-1. Fu, Y., Xie, C., Yan, M., Li, Q., Joh, J.W., Lu, C., Mohan, C. Kidney Int. (2005) [Pubmed]
  9. Renal biopsy collagen I mRNA predicts scarring in rabbit anti-GBM disease: comparison with conventional measures. Lee, S.K., Goyal, M., de Miguel, M., Thomas, P., Wharram, B., Dysko, R., Phan, S., Killen, P.D., Wiggins, R.C. Kidney Int. (1997) [Pubmed]
  10. Adoptive transfer studies demonstrate that macrophages can induce proteinuria and mesangial cell proliferation. Ikezumi, Y., Hurst, L.A., Masaki, T., Atkins, R.C., Nikolic-Paterson, D.J. Kidney Int. (2003) [Pubmed]
  11. Protection against anti-glomerular basement membrane (GBM)-mediated nephritis in C3- and C4-deficient mice. Sheerin, N.S., Springall, T., Carroll, M.C., Hartley, B., Sacks, S.H. Clin. Exp. Immunol. (1997) [Pubmed]
  12. Factors affecting the glomerular protein leak after polyclonal activation in the HgCl2-induced model of anti-GBM disease in the brown Norway rat. Savige, J.A., Lockwood, C.M. Clin. Exp. Immunol. (1987) [Pubmed]
  13. Unusual presentations of anti-glomerular basement membrane antibody mediated disease are associated with delayed diagnosis and poor outcome. Andrews, P.A., Sheerin, N.S., Hicks, J.A., Williams, D.G., Sacks, S.H. Clin. Nephrol. (1995) [Pubmed]
  14. Intrinsic renal cells are the major source of interleukin-1 beta synthesis in normal and diseased rat kidney. Tesch, G.H., Yang, N., Yu, H., Lan, H.Y., Foti, R., Chadban, S.J., Atkins, R.C., Nikolic-Paterson, D.J. Nephrol. Dial. Transplant. (1997) [Pubmed]
  15. Sequence analysis of the 'Goodpasture antigen' of mammals. Ryan, J.J., Katbamna, I., Mason, P.J., Pusey, C.D., Turner, A.N. Nephrol. Dial. Transplant. (1998) [Pubmed]
  16. HLA-DR and -DQ genotyping in anti-GBM disease. Dunckley, H., Chapman, J.R., Burke, J., Charlesworth, J., Hayes, J., Haywood, E., Hutchison, B., Ibels, L., Kalowski, S., Kincaid-Smith, P. Dis. Markers (1991) [Pubmed]
  17. Regulation by CD25+ lymphocytes of autoantigen-specific T-cell responses in Goodpasture's (anti-GBM) disease. Salama, A.D., Chaudhry, A.N., Holthaus, K.A., Mosley, K., Kalluri, R., Sayegh, M.H., Lechler, R.I., Pusey, C.D., Lightstone, L. Kidney Int. (2003) [Pubmed]
  18. Glomerular expression and cell origin of transforming growth factor-beta 1 in anti-glomerular basement membrane disease. Lianos, E.A., Orphanos, V., Cattell, V., Cook, T., Anagnou, N. Am. J. Med. Sci. (1994) [Pubmed]
  19. Susceptibility to anti-glomerular basement membrane disease is strongly associated with HLA-DRB1 genes. Fisher, M., Pusey, C.D., Vaughan, R.W., Rees, A.J. Kidney Int. (1997) [Pubmed]
  20. Heparanase inhibition reduces proteinuria in a model of accelerated anti-glomerular basement membrane antibody disease. Levidiotis, V., Freeman, C., Tikellis, C., Cooper, M.E., Power, D.A. Nephrology (Carlton, Vic.) (2005) [Pubmed]
  21. The ICAM-1/LFA-1 interaction in glomerular leukocytic accumulation in anti-GBM glomerulonephritis. Hill, P.A., Lan, H.Y., Nikolic-Paterson, D.J., Atkins, R.C. Kidney Int. (1994) [Pubmed]
  22. A single autoantigen in Goodpasture's syndrome identified by a monoclonal antibody to human glomerular basement membrane. Pusey, C.D., Dash, A., Kershaw, M.J., Morgan, A., Reilly, A., Rees, A.J., Lockwood, C.M. Lab. Invest. (1987) [Pubmed]
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