title: Infection and glomerulonephritis.
abstract: Glomerular injury, occurring either as primary glomerular disease or as part of a systemic disease process, is usually a result of immune-mediated mechanisms. The morphologic reaction pattern has a diverse spectrum of appearance, ranging from normal by light microscopy in minimal change disease to crescentic forms of glomerulonephritis, with conspicuous disruption of the normal glomerular morphology. The mechanisms of glomerular immune deposit formation include trapping of circulating antigen-antibody complexes and the in situ formation of immune complexes within the glomerulus. While the majority of postinfectious immune-complex-mediated glomerulonephritides are believed to result from the deposition of circulating antigen-antibody complexes, preformed outside of the kidney and secondarily deposited in the kidney, the notion of forming in situ antigen-antibody complexes to either planted antigens or to integral structural components of the glomerulus, through "cross-reacting" autoimmune reactions, is gaining popularity in a variety of forms of glomerulonephritides. Patients with HIV infection may develop a spectrum of renal pathology, the glomerular manifestations of which include both antigen-antibody complex and nonimmune-complex-mediated pathogenetic mechanisms. Similarly, patients with Streptococcal infections, Hepatitis B virus, or Hepatitis C virus infection may develop a spectrum of glomerulonephritides, which are predominantly immune-complex-mediated. Therapy for glomerular diseases due to HIV, hepatitis B, or C virus infections remains a challenge.
authors.affiliation: Division of Nephrology, University of the Witwatersrand, Johannesburg Hospital, 7 York Road, Parktown, Johannesburg, Gauteng, 2193, South Africa. Saraladevi.Naicker@wits.ac.za
authors.forename: Saraladevi
authors.initials: S
authors.lastname: Naicker
authors.forename: June
authors.initials: J
authors.lastname: Fabian
authors.forename: Sagren
authors.initials: S
authors.lastname: Naidoo
authors.forename: Shoyab
authors.initials: S
authors.lastname: Wadee
authors.forename: Graham
authors.initials: G
authors.lastname: Paget
authors.forename: Stewart
authors.initials: S
authors.lastname: Goetsch
mesh_terms: D000818:Animals; D000936:Antigen-Antibody Complex / Q000276:immunology*; D015551:Autoimmunity; D005921:Glomerulonephritis / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007678:Kidney Glomerulus / Q000276:immunology* / Q000473:pathology; D013290:Streptococcal Infections / Q000150:complications / Q000276:immunology* / Q000473:pathology; D014777:Virus Diseases / Q000150:complications / Q000276:immunology* / Q000473:pathology
chemical_list: D000936:Antigen-Antibody Complex