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| Postinfectious Glomerulonephritis |
| Etiology |
•Streptococcal infection (outside the kidney) leads to
immune complex formation. The immune complexes are presumed to form in situ
in the glomeruli due to previously planted streptococcal antigen. •Some strains of streptococci are more likely to result in postinfectious glomerulonephritis (serotypes 1, 4, 12). |
| Pathogenesis |
•Streptococcal antigens from the
infection elicit the production of anti-streptococcal antibodies. •Immune
complexes form in situ in glomeruli due to previously planted streptococcal
antigens. •The immune complex formation with complement activation incites acute glomerular inflammation. |
| Epidemiology |
•Most
cases are in the pediatric age group. •The disease follows a previous (1
to 4 weeks earlier)
infection. •Streptococcal infections are the most common, but other
infectious agents are capable of producing the disease. •Immunogenetics: HLA D 3EN2, •DR4. |
| Clinical |
•Classically, there is a preceeding streptococcal infection such as
pharyngitis or skin infection. •After an interval of several weeks the
patient experiences malaise and notes a dark smoky discoloration of the
urine. •Examination of the urine sediment reveals red cells and red cell
casts. •There may be soft tissue edema (peri-orbital) and hypertension. |
| General Gross Description |
•The kidneys in postinfectious glomerulonephritis may show no particular
gross abnormalities. •In severe cases, the cut surface of the renal cortex may show a petechial or flea-bitten appearance. |
| General Micro Description |
•The glomeruli are
diffusely and globally hypercellular with a predominance of
neutrophils. •The increased cellularity is endocapillary, meaning that
the increase in cells is within the glomerular tuft and there is little if
any proliferation of cells in the urinary space. •Direct
immunofluorescence shows randomly scattered fluorescent granules (starry-sky
pattern) in the glomerular tufts that are positive for IgG and C3. •Electron microscopy shows large rounded subepithelial dense deposits in addition to the proliferative and inflammatory changes. |
| Reference |
• Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 945-947. •Rose B. Renal Pathophysiology the essentials. Baltimore: Williams and Wilkins. 1994. Ch. 9.
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