Crescentic glomerulonephritis is a rare complication of AA amyloidosis. There are no clinical case reports of this complicating AL amyloidosis. A 67-year-old man developed rapidly progressive glomerulonephritis (RPGN) on a background of primary AL amyloidosis and IgGkappa multiple myeloma. Investigations for causes of glomerulonephritis were negative, and a renal biopsy confirmed crescentic glo...

Crescentic glomerulonephritis is characterized by glomerular fibrin deposition, and experimental crescentic glomerulonephritis has been shown to be fibrin-dependent. Net fibrin deposition is a balance between activation of the coagulation system causing glomerular fibrin deposition and fibrin removal by the plasminogen-plasmin (fibrinolytic) system. Plasminogen activator inhibitor-1 (PAI-1) inh...

introduction antineutrophil cytoplasmic antibodies (anca)-associated glomerulonephritis (gn) is characterized by necrotizing and crescentic gn with paucity of immunoglobulin (ig) and complement deposition, which is also known as pauci-immune crescentic gn. membranous nephropathy (mn) is characterized by the formation of subepithelial immune deposit with resultant changes in glomerular basement ...

A 43-year-old woman with rheumatoid arthritis (RA), renal amyloidosis and crescentic glomerulonephritis had severe abdominal pain, melena and progressive renal failure. Autopsy findings revealed vasculitis of small and middle size of vessels and there was a deposition of amyloid in the small intestines. Although there were no findings of vasculitis in the kidney, amyloid deposition was noticed ...

Most humans with microscopic polyarteritis and anti-myeloperoxidase (anti-MPO), anti-neutrophil cytoplasmic antibodies (ANCA) develop "pauci-immune" crescentic glomerulonephritis. For dissection of the roles of ANCA and cell-mediated effectors in microscopic polyarteritis, experimental autoimmune anti-MPO glomerulonephritis was induced by immunizing C57BL/6 mice with human MPO. Autoimmunity to ...