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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. |
| 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 Microscopic 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. |
| Clinical Correlation •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. |
| References • 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. |
| Postinfectious Glomerulonephritis |
| Synopsis by: Harold Yamase M.D. (T71200M00096)[217] |
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