Observations on the evolution of idiopathic rapidly progressive glomerulonephritis.
Distinctive deposits of C3, C5 and properdin were identified in the minimally proliferative glomerular lesions of a patient with idiopathic rapidly progressive glomerulonephritis. Biopsies of her renal allograft at times of recurrences of her disease and of five other patients with progressive renal failure but less severe crescent formation showed deposits identical composition and position, giving evidence of a common pathogenesis. The deposits were subepithelial and located in that part of the basement membrane in apposition to the mesangium (capillary waist). Breaks in the basement membrane were often exclusively in this area suggesting the deposits were causative. Ancillary observations suggest that the subepithelial deposits become unidentifiable after the scarring of severe extracapillary proliferation develops. Three of the patients had, in addition, intramembranous dense deposits but in other ways their disease was not characteristic of membranoproliferative glomerulonephritis Type II. Instead, the evidence indicated that all six patients were in early or lage stages of idiopathic (non-streptococcal) rapidly progressive glomerulonephritis.
D001485:Basement Membrane / Q000648:ultrastructure; D002648:Child; D002675:Child, Preschool; D003176:Complement C3; D003182:Complement C5; D005260:Female; D005921:Glomerulonephritis / Q000209:etiology* / Q000276:immunology / Q000628:therapy; D006801:Humans; D007678:Kidney Glomerulus / Q000648:ultrastructure; D016030:Kidney Transplantation; D008297:Male; D011414:Properdin; D014184:Transplantation, Homologous
D003176:Complement C3; D003182:Complement C5; D011414:Properdin