On the pathogenesis of glomerulonephritis: a clinico-pathological study indicating that neutrophils attack and degrade glomerular basement membrane.
Lysosomal proteinase activity was assayed in urines from 157 patients with renal disease. 16 were found to be excreting acid and neutral proteinases. 15 of these 16 had a severe proliferative glomerulonephritis with polymorphonuclear leucocyte (PMN) infiltration of the glomeruli. These same 16 patients excreted excess quantities of glomerular basement membrane (GBM) antigen. Only urines with neutral proteinase activity were capable of degrading GBM in vitro. Clinical recovery was accompanied by disappearance of both proteinases and excess GBM fragments from the urine. Detailed studies on one patient showed that the neutral proteinase activity was, at least in part, due to PMN lysosomal elastase. Calculation shows that in these patients enough PMN neutral proteinase was present in the glomeruli to cause significant GBM damage.
D000941:Antigens / Q000652:urine; D001485:Basement Membrane / Q000276:immunology / Q000473:pathology*; D010450:Endopeptidases / Q000032:analysis / Q000652:urine; D005921:Glomerulonephritis / Q000209:etiology / Q000276:immunology / Q000473:pathology*; D006801:Humans; D006909:Hydroxyproline / Q000652:urine; D066298:In Vitro Techniques; D007678:Kidney Glomerulus / Q000276:immunology / Q000473:pathology*; D009504:Neutrophils / Q000201:enzymology* / Q000473:pathology; D010196:Pancreatic Elastase / Q000032:analysis / Q000652:urine
D000941:Antigens; D010450:Endopeptidases; D010196:Pancreatic Elastase; D006909:Hydroxyproline