3. 1.What is the immunological mechanism leading to the
glomerulonephritis?
• Actually Before going into the immunological mechanism of
glomerulonephritis, first of all we need to know what is
Glomerulonephritis.
What is glomerulonephritis?
Glomerulonephritis (GN) is inflammation of the glomeruli, which are structures in your kidneys that
are made up of tiny blood vessels. These knots of vessels help filter your blood and remove excess
fluids. If your glomeruli are damaged, your kidneys will stop working properly, and you can go into
kidney failure.
Sometimes called nephritis, GN is a serious illness that can be life-threatening and requires
immediate treatment. GN can be both acute, or sudden, and chronic, or long-term. This condition
used to be known as Bright's disease.
Now, lets move onto the actual mechanism behind glomerulonephritis
4. Type III example – glomerulonephritis
Membranous glomerulonephritis is a
common lesion produced by Type III
immune-complex hypersensitivity.
Immune complexes may be deposited
or formed on the capillary or
mesangial side of glomerular
basement membrane. The mechanism
of tissue damage is mediated by
neutrophils. In addition, the physical
presence of immune complexes
interferes with filtration and causes
fusion of foot processes of glomerular
epithelial cells disrupting glomerular
filtration and later interfering with
blood flow through the glomerulus.
5. Type III hypersensitivity
• The third type of immunologic injury, (Type III), is also called immune-complex
mediated hypersensitivity.
• Like Type I and Type II reactions, Type III reactions depend on initial exposure to
an antigen, and production of immunoglobulin against that antigen.
• If the concentrations of the antigen and IgG or IgM are just right (slight antigen
excess), soluble antigen-antibody complexes are formed.
• Immune complex disease is seen in persistent infectious diseases and in
autoimmune disease.
• Immune complex-mediated disorders can be generalized, involving the blood
vessels of many organs (acute serum sickness), or may be localized to the kidney
(glomerulonephritis), joints, (arthritis), or to the small blood vessels of the skin.
• At any of the sites, however, the deposition of antigen-antibody complex results
in activation of the complement cascade, chemotaxis of neutrophils, release of
neutrophil digestive enzymes and oxygen radicals and eventual tissue injury.
• Also, the complexes alter the negative charge of the basement membrane,
allowing small proteins to pass through.
6. Some of the clinicopathologic manifestations of
Glomerulonephritis {GN} are
• 1. Good pasture’s syndrome
• 2. Post –streptococcal glomerulonephritis
• 3. Serum sickness
• 4. Systemic lupus erytheromatosus [SLE]
• 1. Good pasture’s syndrome
• Goodpasture's syndrome is an auto-immune, hypersensitivity disorder of
unknown cause characterized by circulating anti-glomerular basement
membrane antibodies and linear deposition of immunoglobulin and
complement in the glomerular basement membrane.
7. 2. Systemic lupus erythematosus
Systemic lupus erythematosus (SLE) is a complex disease characterized by the appearance of
autoantibodies against nuclear antigens and the involvement of multiple organ systems,
including the kidneys. Loss of B-cell tolerance is a hallmark feature of the pathogenesis in
systemic lupus erythematosus (SLE), an autoimmune disease that is characterized by
hypergammaglobulinemia and autoantibody production.The precise immunological events that
trigger the onset of clinical manifestations of SLE are not yet well understood. lupus nephritis
(also known as SLE nephritis) is an inflammation of the kidneys caused by systemic lupus
erythematosus (SLE), an autoimmune disease. It is a type of glomerulonephritis in which the
glomeruli become inflamed.
• 3. Post –streptococcal glomerulonephritis
• Acute glomerulonephritis that results from streptococcal infections is the
best-studied immune complex-mediated glomerulonephritis.In-situ formation
of immune complexes is a characteristic associated with cationic antigens that
have a charge-facilitated penetration through the polyanionic glomerular
basement membrane
8. 4. Serum sickness
Disease caused by the injection of large doses of protein antigen into the blood and characterized by
the deposition of antigen antibody {immune complexes}in the blood vessel walls, especially in the
kidney and joints. Immune complex deposition leads to complement fixation and leukocyte
recruitment and subsequently to glomerulonephritis and arthritis .Serum sickness was originally
described as a disorder that occurred in patients receiving injections of serum containing antitoxin
antibodies to prevent diphtheria.
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