This is a group of diseases in which the disease affects the glomerulus and is often inflammatory in nature.
The disease is immunologically mediated and involves both kidneys symmetrically.
It may be primary when the major problem starts in the glomerulus or secondary when involvement is part of systemic disease such as in SLE.
• Minimal change glomerular disease
• Membranous glomerulonephritis
• Membranoproliferative glomerulonephritis
• IgA nephropathy
• Crescentric (Goodpasture’s Syndrome)
• Focus segmental glomerulonephritis
• Polyarteritis nodosa
• Diabetes mellitus
• Henoch Schontein disease
• Malarial nephropathy
• Malignancy associated Paraproteinamea
• Rheumatoid arthritis
• Hemolytic uremic syndrome
• Wegner’s granulomatosis
• Cytomegalovirus nephropathy
• AIDS nephropathy
The two main processes are involved in the aggregation, inflammation with inflammatory pathogenesis of glomerulonephritis. cytokines and free radical-induced damage.
This is the most common mechanism of glomerulonephritis.
Circulating antigen-antibody complexes are deposited in the kidney or complexes are formed locally when circulating free antigen has become trapped in the glomerulus, when they produce injury through the binding of the complement system.
The antigen may be exogenous e.g. bacteria (group A beta-hemolytic streptococci cause glomerulonephritis) or endogenous e.g. in SLE in which antibodies against host DNA are produced.
Antibodies (anti-glomerular basement membrane) react with an antigen in the glomerular base membrane & produce glomerulonephritis.
This mechanism is responsible for < 5% cases of glomerulonephritis. An example is Goodpasture’s syndrome.
Glomerulonephritis presents in one of the four ways
1 . Asymptomatic proteinuria and/or microscopic hematuria – discovered on routine medical examination.
2. Acute nephritic syndrome.
3. Nephrotic syndrome: it may be pure nephrotic or mixed nephrotic/nephritic syndrome.
4. Rapidly progressive glomerulonephritis.