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Glomerulonephritis is a primary or secondary autoimmune renal disease featuring inflammation of the glomeruli. It may be asymptomatic, or present with hematuria and/or proteinuria (blood resp. protein in the urine). There are many recognised types, divided in acute, subacute or chronic glomerulonephritis. Causes are infectious (bacterial, viral or parasitic pathogens), autoimmune or paraneoplastic.
Acute diffuse proliferative GN
Histopathology: the majority of glomeruli present hypercellularity due to proliferation of endothelial and mesangial cells, inflammatory infiltrate with neutrophils and with monocytes. The Bowman space is reduced (compressed). Tubules are not affected.
Rapidly progressive GN (Crescentic GN)
Histopathology: The majority of glomeruli present "crescents". Formation of crescents is initiated by passage of fibrin into the Bowman space as a result of increased permeability of glomerular basement membrane. Fibrin stimulates the proliferation of parietal cells of Bowman capsule, and an influx of monocytes. Rapid growing and fibrosis of crescents compresses the capillary loops and decreases the Bowman space which leads to renal failure within weeks or months.
Mesangial proliferative GN
This type is due to deposition of polymerised IgA1 in the mesangium , with a localised proliferation of tissue. It is consistent with IgA nephritis (Berger's disease) and usually presents with macroscopic hematuria.
Minimal change GN
This form of GN usually (though not exclusively) presents in children with nephrotic syndrome and massive proteinuria. It is controlled with steroids. As the name indicates, there are no changes on light microscopy.
Chronic glomerulonephritis represents the end-stage of all glomerulonephritis with unfavorable evolution.
Histopathology: few glomeruli may still present changes which permit to discern the etiology of CGN. The majority of the glomeruli are affected. Depending on the stage of the disease, they may present different degrees of hyalinization (hyalinosclerosis - total replacement of glomeruli and Bowman's space with hyaline). The hyaline is an amorphous material, pink, homogenous, resulted from combination of plasma proteins, increased mesangial matrix and collagen. Totally hyalines glomeruli are atrophic (smaller), lacking capillaries, hence non-functional. Obstruction of blood flow will produce secondary tubular atrophy, interstitial fibrosis and thickening of the arterial wall by hyaline deposits. Functional nephrons have dilated tubules, often with hyaline casts in the lumens. In the interstitium is present an abundant inflammatory infiltrate (mostly with lymphocytes).
This general (glomerular, vascular and interstitial) affection constitutes the so-called "end stage kidney". In most cases, it is associated with systemic hypertension.
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