Acute Proliferative Glomerulonephritis
| Overview |
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- Acute Proliferative Glomerulonephritis (APGN) is a disease characterized by a unique histopathology that can manifest clinically as nephritic syndrome. A number of distinct agents can cause APGN but the pathogenesis of all appears to involve generation of circulating immune complexes. The prototypical etiology of APGN is pharyngeal or dermatological infection with certain strains of streptococci (especially beta-hemolytic strains), and thus APGN is often termed "Poststreptococcal Glomerulonephritis".
| Morphology |
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- Light Microscopy
- APGN is characterized by diffuse proliferation of mesangial cells and glomerular capillary endothelial cells in nearly all glomeruli. Glomeruli also display an inflammatory infiltration of neutrophils and macrophages.
- Immunofluorescence
- APGN displays a granular deposition of IgG and complement within the glomerular barrier, suggesting presence of immune complexes.
- Electron Microscopy
- Clumps of immune complexes can be observed in various locations throughout the glomerular basement membrane. Clumps may appear under the podocytes (termed 'subepithelial') or under the glomerular capillaries (termed 'subendothelial').
| Pathogenesis |
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- APGN is ultimately the result of the formation of immune complexes within the glomerular basement membrane along with activation of complement. However, it is not clear if immune complexes are "preformed" or develop "in situ" (See: Basic Glomerular Pathogenesis). Whatever their origin, deposition of immune complexes initiates inflammation of glomeruli, thus precipitating subsequent pathogenesis of nephritic syndrome (see page). The source of the antigen precipitating creation of immune complexes can be both from an exogenous infectious agent or from an endogenous antigen. The prototypical infectious agent which precipitates APGN is streptococci whereas endogenous immune complexes released during evolution of Systemic Lupus Erythematosus can act as a culprit.
| Clinical Consequences |
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- APGN typically presents with the signs of nephritic syndrome characterized by hematuria, pyuria, secondary hypertension, oliguria, and azotemia. However, significant proteinuria reminiscent of nephrotic syndrome can also occur. constitutional symptoms are also frequently present. If severe, the disease can progress to the much more serious syndrome of rapidly progressive glomerulonephritis; however, most cases spontaneously resolve and prognosis is good.
| Epidemiology |
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- APGN can occur in both adults and children; however, post-streptococcal etiologies are much more common in children.