title: Mesangiocapillary glomerulonephritis.
abstract: The clinical and histological features of idiopathic mesangiocapillary glomerulonephritis (MCGN) have been reviewed, with a survey of the most recent literature, including the retrospective analysis of the data of the Italian Study Group of Renal Immunopathology on 368 patients. In both major types of MCGN, six morphological variants have been characterized (classical MCGN, nodular MCGN, exudative MCGN, focal segmental MCGN, MCGN with massive deposits, and crescentic MCGN) that have different etiologic, pathogenetic, or clinical outcome correlates. Actuarial renal survival 10 yr after renal biopsy has been calculated with life-table analysis to be 60 to 65% in type I MCGN, without significant differences between treated and untreated patients; none of the therapeutic regimens tested up to now for this disease have been independently demonstrated to be efficacious. As for the pathogenesis, the interrelationships between the three mechanisms that contribute to the development of the morphological features of the disease (accumulation of electron-dense deposits on the subendothelial side of the glomerular basement membrane or within the glomerular basement membrane; mesangial proliferation and peripheral interposition; and inflow of inflammatory cells, mainly monocytes) have been discussed, and the role of hypocomplementemia and circulating nephritic factors (NFa and NFt) has been analyzed. Available evidence suggests that MCGN is an immunocomplex-mediated disease, the deposition of immune deposits being the initiating phenomenon, whereas the morphologic changes and complement system activation are secondary events.
authors.affiliation: Division of Nephrology, San Carlo Borromeo Hospital, Milano, Italy.
authors.forename: G
authors.initials: G
authors.lastname: D'Amico
authors.forename: F
authors.initials: F
authors.lastname: Ferrario
mesh_terms: D003165:Complement System Proteins / Q000172:deficiency; D015432:Glomerulonephritis, Membranoproliferative / Q000145:classification / Q000209:etiology / Q000473:pathology*; D006801:Humans; D007105:Immune Complex Diseases / Q000209:etiology
chemical_list: D003165:Complement System Proteins