Glomerulonephritis Dr. Abdelaty Shawky Dr. Gehan mohamed.

Glomerulonephritis

Dr. Abdelaty Shawky Dr. Gehan mohamed

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• 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, sub-endothelial, 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.

30RBCs cast

Hematuria (coca cola colored urine)

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• 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.