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Goodpasture syndrome (GPS), also known as anti–glomerular basement membrane disease, is a rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from the lungs, glomerulonephritis, [1] and kidney failure. [2]
Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of kidney function, [4] [5] (usually a 50% decline in the glomerular filtration rate (GFR) within 3 months) [5] with glomerular crescent formation seen in at least 50% [5] or 75% [4] of glomeruli seen on kidney biopsies.
The linear and granular patterns are examples of positive immunofluorescence that are associated as follows: Goodpasture syndrome (linear pattern), post-streptococcal glomerulonephritis (granular), and diffuse proliferative nephritis (granular). [1]
Membranoproliferative glomerulonephritis (MPGN) is a type of glomerulonephritis caused by deposits in the kidney glomerular mesangium and basement membrane thickening, [2] activating the complement system and damaging the glomeruli.
Anti-glomerular basement membrane antibody (anti-GBM Ab) is an antibody which is found in Goodpasture's syndrome but not found in microscopic polyangiitis.. Some sources consider "anti-GBM disease" and "Goodpasture disease" to be synonymous terms describing histological presentation, reserving the term "Goodpasture syndrome" for clinical presentation.
Goodpasture syndrome [ edit ] The alpha-3 subunit (COL4A3) of collagen IV is thought to be the antigen implicated in Goodpasture syndrome , wherein the immune system attacks the basement membranes of the glomeruli and the alveoli upon the antigenic site on the alpha-3 subunit becomes unsequestered due to environmental exposures.
The glomerular basement membrane of the kidney is the basal lamina layer of the glomerulus.The glomerular endothelial cells, the glomerular basement membrane, and the filtration slits between the podocytes perform the filtration function of the glomerulus, separating the blood in the capillaries from the filtrate that forms in Bowman's capsule. [1]
Hemosiderin deposition in the lungs is often seen after diffuse alveolar hemorrhage, which occurs in diseases such as Goodpasture's syndrome, granulomatosis with polyangiitis, and idiopathic pulmonary hemosiderosis. Mitral stenosis can also lead to pulmonary hemosiderosis. Hemosiderin collects throughout the body in hemochromatosis.