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glomerular basement membrane (GBM) autoantibodies 295 glomerulonephritis (GN)
Bruce Glick.
(pseudoglobulins). Globulins are precipitated in half-saturated
ammonium sulfate solution.
Glomerular basement membrane (GBM) autoantibodies.
glomerular basement membrane (GBM) autoantibodies
Autoantibodies against the noncollagenous portion (NC1)
of the α3 chain of type IV collagen present in both GBM
and alveolar basement membranes are revealed by enzyme
immunoassay (EIA) in Goodpasture’s syndrome. NC1 antibodies
comprise 1% of the total immunoglobulin M (IgM)
in patients with this syndrome, and 90% of these autoantibodies
are specific for the α3 (IV) chain. Antibodies to the
other α (IV) chains occur in 80% of the patients. Both CXC
and CC chemokines are associated with glomerular polymorphonuclear
neutrophil and monocyte/macrophage infiltration
in glomerulonephritis induced by GBM antibody.
Sixty percent of human anti-GBM nephritis patients reveal
antibody deposits along tubule basement membranes and
manifest tubulointerstitial injury. Ten to 35% of patients
with Goodpasture’s syndrome develop pANCA with
myeloperoxidase antibody activity. ANCA and GBM
antibodies may appear together in the sera of patients with
rapidly progressive glomerulonephritis (RPGN) associated
with GBM disease and systemic vasculitis.
Normal Proliferative GN
Membranous GN
Types of glomerulonephritis.
Glomerulonephritis (GN).
Membranoproliferative GN
glomerulonephritis (GN)
A group of diseases characterized by glomerular injury.
Immune mechanisms are responsible for most cases of primary
glomerulonephritis and many of the secondary glomerulonephritis
group. More than 70% of glomerulonephritis
patients have glomerular deposits of immunoglobulins,
frequently with complement components. Antibodyassociated
injury may result from the deposition of soluble
circulating antigen–antibody complexes in the glomerulus
or by antibodies reacting in the glomerulus with antigens
intrinsic to the glomerulus or with molecules planted within
the glomerulus. Cytotoxic antibodies may also cause glomerular
injury. Goodpasture’s syndrome is an example of a
disease in which antibodies react directly with the glomerular
basement membrane, interrupting its integrity and
permitting red blood cells to pass into the urine. Antigen–
antibody complexes such as those produced in systemic
lupus erythematosus (SLE) may be deposited in the walls of
the peripheral capillary loops, especially in subendothelial
locations, leading to various manifestations of glomerulonephritis,
depending on the stage of the disease. In membranoproliferative
glomerulonephritis type I, IgG and C3 are
found deposited in the glomerulus, whereas in dense deposit
G