Glomerulonephritis
Dr. Abdelaty Shawky Dr. Gehan mohamed
• Glomerular diseases constitute some of the major
problems in nephrology; indeed, chronic
glomerulonephritis is one of the most common
causes of chronic renal failure in humans.
• Glomeruli may be injured by a variety of factors and
in the course of a number of systemic diseases.
Systemic immunologic diseases such as systemic
lupus erythematosus (SLE), hypertension and
polyarteritis nodosa, diabetes mellitus, often affect
the glomerulus.
• These are termed secondary glomerular diseases to
differentiate them from disorders in which the
kidney is the only or predominant organ involved.
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* Classification of glomerular diseases:
I. Primary G.N (the disease affects kidney only):
• Minimal change glomerular disease (Lipoid nephrosis).
• Acute diffuse proliferative G.N:
– Post-streptococcal G.N.
– Non-post-streptococcal GN.
• Rapidaly progressive G.N.
• Membraneous G.N.
• Membranoproliferative G.N.
• Chronic G.N.
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II. Secondary G.N (the disease affects kidney and
other organs):
– Systemic lupus erythematosus (SLE).
– Polyarteritis nodosa (PAN).
– Wegener granulomatosis.
– Diabetes mellitus (diabeteic nephropathy).
– Goodpasture syndrome.
– Amyloidosis.
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Normal Glomerulus
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• Most of the 1ry glomerular disease are due to
immunologic mechanisms.
• To study any glomerular disease, a renal biopsy is
taken and examined by 3 types of microscopes:
1. Light microscope: to examine the structure of
glomeruli, tubules and interstitium.
2. IF (immune flourescent microscope): to detect the
type of deposited immunoglobulin in the glomeruli.
3. EM (electron microscope): to detect the site of
immune complex, either sub-epithelial, subendothelial, mesangial or basement membrane..
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Minimal change glomerular disease
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*Etiology & pathogenesis:
• Chemical change in the glomerular basement
membrane causing protein loss.
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* Grossly:
• Mild bilateral kidney enlargement.
* LM (Light microscope):
• No abnormalities.
* IF (Immunoflurescence):
• No immune deposits.
* EM (Electron microscope):
• Fusion of the foot processes of the epithelial cells
(podocytes).
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EM of normal glomerulus
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EM of minimal change glom. disease
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* CP (Clinical picture):
• Affect children and young adults.
• Cause nephrotic syndrome.
* Fate:
• The disease has excellent prognosis and most
patients respond to corticosteroids with
complete resolution of proteinuria.
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Post-streptococcal G.N
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*Etiology & pathogenesis:
• Immune complex reaction; (nephrotegenic
strains of group A beta haemolytic
streptococci + Ig G), the complex is deposited
in the glomeruli with subsequent complement
activation  acute inflammation.
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* Grossly:
• Mild bilateral kidney enlargement with
petechial haemorrhages.
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* LM (Light microscope):
a. Glomeruli:
• Proliferation of endothelial and mesangial cells.
• Glomerular capillaries contain neutrophils.
• Bowman’s space shows: neutrophils, RBCs, some
albumin.
b. Tubules:
• The lining cells are swollen.
• The lumens show casts (RBCs casts, neutrophil
casts & hyaline casts).
c. Interstitium:
• Acute inflammatory reaction…...
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Normal kidney
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Normal kidney
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Post-streptococcal GN
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Post-streptococcal GN
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Post-streptococcal GN
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Post-streptococcal GN
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* IF (Immunoflurescence):
• Deposition of Ig G and C3.
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Positive Ig G and C3
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* EM (Electron microscope):
• Subepithelial immune complex deposit (humps).
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* CP (Clinical picture):
• In the classic case, a young child abruptly
develops malaise, fever, nausea, oliguria, and
hematuria (smoky or cocoa-colored urine) 1 to 2
weeks after recovery from a sore throat.
• The patients exhibit red cell casts in the urine,
mild proteinuria (usually less than 1 mg/day),
peri-orbital edema, and mild to moderate
hypertension.
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Hematuria (coca
cola colored urine)
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RBCs cast
• In adults, the onset is more likely to be atypical,
with the sudden appearance of hypertension or
edema, frequently with elevation of serum
creatinine. Important laboratory findings include
elevations of anti-streptococcal antibody (ASO)
titers and a decline in the serum concentration
of C3 (consumed).
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• More than 95% of affected children eventually
recover totally with conservative therapy aimed
at maintaining sodium and water balance.
• A small minority of children (perhaps less than
1%) do not improve, become severely oliguric,
and develop a rapidly progressive
glomerulonephritis.
• Some of the remaining patients may undergo
slow progression to chronic glomerulonephritis.
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• In adults, the prognosis is bad. Most of the
patients pass to rapidly progressive
glomerulonephritis or chronic renal failure.
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Nephritic syndrome
- A syndrome formed of:
1. Haematuria.
2. Oliguria.
3. Peri-orbital oedema.
4. Hypertension.
- The most common cause of nephritic syndrome
in children is post-streptococcal GN.
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Nephrotic syndrome
- A syndrome formed of:
1. Hypoproteinaemia.
2. Proteinuria .
3. Oedema.
4. Hypercholesterolaemia.
- The most common cause of nephrotic syndrome
in children is minimal change glomerular
disease.
- The most common cause of nephrotic syndrome
in adults is membranous GN.
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Thanks
References:
Robbins and Cotran’s:
Pathologic Basis of Disease.
Seventh edition.
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