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| Membranous Glomerulonephritis |
| Etiology •Most cases of membranous glomerulonephritis (85%) are idiopathic and the etiology is unknown. •Membranous glomerulonephritis can be caused by malignancies, especially carcinomas, hepatitis B infections and lupus. |
| Pathogenesis •Idiopathic membranous glomerulonephritis is believed to occur by in-situ immune complex formation. •Native or foreign antigens planted in the glomerular basement membranes are present beforehand and antibodies to these antigens combine with them in situ to form immune complexes. •The resultant presence of immune complexes alters the permeability of the capillary loops leading to proteinuria., |
| Epidemiology •For idiopathic membranous glomerulonephritis, the disease is more common in adults usually in the fifth to seventh decades of life. •Male to female ratio is approximately 3:1. •Immunogenetics: DR3. |
| General Gross Description •The kidneys in membranous glomerulonephritis show no gross abnormalities in the early phases of the disease. •If the disease persists and glomeruli become sclerosed, the parenchymal mass will decrease and the kidneys will appear small and shrunken. |
| General Microscopic Description •The glomerular capillary loops are thickened. •The longer the existence of the disease, the thicker the capillary loops become. •The glomeruli otherwise show normocellularity and the capillary loops are patent. •On the PAM silver stain, spike-like projections are seen extending outward from the glomerular capillary basement membranes. •Direct immunofluorescence studies show granular capillary loop fluorescence for IgG and C3. •Electron microscopy shows numerous subepithelial electron dense deposits. These deposits are seen virtually in every glomerulus and every loop. |
| Clinical Correlation •Patients with membranous glomerulonephritis manifest heavy proteinuria (3.5 gm or more per 24 hours) and the consequence of protein loss (hypoalbuminemia, hyperlipidemia, edema). •Some complications of heavy proteinuria include increased vulnerability to infections and increased risk of thrombotic and thromboembolic diseases. |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 949-50. •Rose B. Renal Pathophysiology the essentials. Baltimore: Williams and Wilkins. 1994. Ch. 9. |
| Membranous Glomerulonephritis |
| Synopsis by: Harold Yamase M.D. (T71200M00016)[215] |
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