IgA Nephropathy
| Overview |
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- IgA Nephropathy is characterized by episodic manifestation of nephritic syndrome in some cases quickly following a upper respiratory infection.
| Etiopathogenesis |
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- Although the precise etiology and pathogenesis of IgA nephropathy is not known, an acquired dysregulation of IgA is suspected. Whatever the cause, IgA becomes deposited in the mesangium and activates complement. This ultimately leads to inflammation of the glomerulus, initiating the pathogenesis of nephritic syndrome (See page for further details). Because of the prominent role of IgA in its pathogenesis and its post-infectious initiation, IgA Nephropathy may be a variant of Henoch-Schonlein Purpura.
| Morphology |
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- Light Microscopy
- IgA nephropathy can appear in a variety of glomerular histopathological forms. Whatever the morphology, proliferation of mesangial cells is usually seen along with focal or diffuse inflammation of glomeruli.
- Immunofluorescence
- The presence of IgA is seen throughout the mesangium along with complement.
| Clinical Consequences |
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- IgA Nephropathy usually presents with signs of nephritic syndrome (i.e. hematuria, pyuria, secondary hypertension, oliguria, and azotemia). These signs and symptoms occur in episodes lasting a few days and can reappear several months later. However, the disease rarely progresses to more serious renal failure.
| Epidemiology |
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- IgA nephropathy is an extremely common cause of glomerulonephritis around the world and is usually observed in younger adults in the second and third decade.