title: [Glomerulonephritis].
abstract: In glomerulonephritis we find various anatomical and pathological aspects of the kidneys, despite the clinical manifestations are almost identical (haematuria, proteinuria, nephrotic or nephritic syndrome). The anatomical damage and the clinical manifestations is produced by a known or unknown antigenic insult, in relation to the predisposing genetic factors and to the defences predisposed by the immunological system. From the '80, some publications showed an immunological pathogenesis of the glomerulonephritis, with the participation of haematological elements such as lymphoid cells. Therefore, the pathogenesis of the primitive glomerulonephritis are in great part unknown, although we know that the increased permeability of the glomerular capillary is correlated to the production of proinflammatory lymphokines from T cells, which are overexpressed (RANTES). Not to succeed to adequately eliminate these cells can be, thus, a cause of relapse with the final result of renal infiltration and amplification of the immune response.
authors.forename: G E
authors.initials: GE
authors.lastname: Russo
authors.forename: A
authors.initials: A
authors.lastname: Morgia
authors.forename: M
authors.initials: M
authors.lastname: Cavallini
mesh_terms: D018946:Chemokine CCL5 / Q000378:metabolism; D005921:Glomerulonephritis / Q000150:complications / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D006417:Hematuria / Q000209:etiology; D006801:Humans; D009404:Nephrotic Syndrome / Q000209:etiology; D011507:Proteinuria / Q000209:etiology
chemical_list: D018946:Chemokine CCL5