Glomerulonephritis or Glomerulonephritides is a serious renal case which has different presentations .
In this article we are going to illustrate the mechanism and the known presentations ( syndromes ) of G.N
Definition:
Glomerulonephritis is an immune mediated glomerular injury with symmetrical simultaneous involvement of both kidneys at the same time.
• In situ formation of immune complex.
• Antiglomerular basement membrane antibody (anti-GBM) e.g. Good pasture syndrome.
The above mechanisms activate secondary mechanisms that produce glomerular damage.
Secondary mechanisms of glomerular injury
• Complement activation.
• Fibrin deposition.
• Platelet aggregation.
• Activation of kinin system.
• Inflammation with neutrophil dependent mechanisms.
Immune complex or anti GBM antibody deposttion trigger the above secondary mechanisms resulting in an increase in capillary permeability and
glomerular damage .
- It may be pure nephrotic syndrome with bland sediment or mixed nephrotic / nephritic syndrome with active sediment
Nephronal hematuria (RBCs cast and / or dysmorphic RBCs) with renal failure developing over weeks to months and diffuse glomerular crescents.
- Hematuria (with or without proteinuria) e.g. in IgA nephropathy and Alpert's syndrome.
e. Chronic Glomerulonephritis
In this article we are going to illustrate the mechanism and the known presentations ( syndromes ) of G.N
Definition:
Glomerulonephritis is an immune mediated glomerular injury with symmetrical simultaneous involvement of both kidneys at the same time.
Mechanism of glomerular injury:
• Circulating Immune complex.• In situ formation of immune complex.
• Antiglomerular basement membrane antibody (anti-GBM) e.g. Good pasture syndrome.
The above mechanisms activate secondary mechanisms that produce glomerular damage.
Secondary mechanisms of glomerular injury
• Complement activation.
• Fibrin deposition.
• Platelet aggregation.
• Activation of kinin system.
• Inflammation with neutrophil dependent mechanisms.
Immune complex or anti GBM antibody deposttion trigger the above secondary mechanisms resulting in an increase in capillary permeability and
glomerular damage .
Glomerular Syndromes ( Presentations of Glomerulonephritis )
a. Acute Nephritic syndrome
Nephronal hematuria (RBC casts and/or dysrnorphlc RBCs) temporarily associated with renal impairment or acute renal failure.b. Nephrotic syndrome
Heavy proteinuria( > 3.5 gm/D/1.73m2).- It may be pure nephrotic syndrome with bland sediment or mixed nephrotic / nephritic syndrome with active sediment
c. Rapidly Progressive Glomerulonephritis
d. Asymptomatic urinary abnormalities:
- Isolated proteinuria ( < 2 gm/D/1.73m2).- Hematuria (with or without proteinuria) e.g. in IgA nephropathy and Alpert's syndrome.
e. Chronic Glomerulonephritis