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An update on glomerulopathies : etiology and pathogenesis by Sharma S Prabhakar

By Sharma S Prabhakar

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2005). , 2011). It is still not clear if C3NeF is directly nephritogenic or it rather appears due to a prolonged or increased presence of the C3 convertase enzyme and complement activation fragments in plasma. Nevertheless, once present, C3NeF by stabilizing the convertase further contributes to an abnormally increased complement activation. As the animal models demonstrated, the generated C3 fragments are involved in glomerular injury, without the requirement of terminal pathway activation, although the latter (also increased by most C3NeFs) exacerbates glomerular inflammation and damage.

N Engl J Med, Vol. 361, No. 1, (Jul 2009), pp. 11-21, ISSN 1533-4406 Bruschi, M; Candiano, G; Murtas, C; Prunotto, M; Santucci, L; Carnevali, ML; Scolari, F; Allegri, L & Ghiggeri, GM. (2009). Patients with primary membranous nephropathy lack auto-antibodies against LDL receptor, the homologue of megalin in human glomeruli. 1093/ndtplus/sfp002 Bruschi, M; Carnevali, ML; Murtas, C; Candiano, G; Petretto, A; Prunotto, M; Gatti, R; Argentiero, L; Magistroni, R; Garibotto, G; Scolari, F; Ravani, P; Gesualdo, L; Allegri, L & Ghiggeri GM.

Clin Exp Immunol, Vol. 118, No. 3, (Dec 1999), pp. 445-50, ISSN 0009-9104 Wistow, GJ; Lietman, T; Williams, LA; Stapel, SO; de Jong, WW; Horwitz, J & Piatigorsky, J. (1988). Tau-crystallin/alpha-enolase: one gene encodes both an enzyme and a lens structural protein. J Cell Biol, Vol. 107, No. 6 Pt 2, (Dec 1988), pp. 2729-2736, ISSN 0021-9525 3 Anti-Complement Autoantibodies in Membranoproliferative Glomerulonephritis and Dense Deposit Disease Mihály Józsi Junior Research Group Cellular Immunobiology, Leibniz Institute for Natural Product Research and Infection Biology, Jena Germany 1.

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