Acute glomerulonephritis
Acute diffuse proliferative GN
Histopathology: a majority of glomeruli present hypercellularity due to proliferation of endothelial & mesangial cells, inflammatory infiltrate by having neutrophile & by having monocytes. A Archer space is reduced (compressed). Tubules are non affected.

Rapidly progressive GN (Crescentic GN)
Histopathology: A majority of glomeruli present "crescents". Formation of crescents is initiated by passage of fibrin into a Archer space following of increased permeableness of glomerular basement membrane. Fibrin causes a proliferation of parietal cells of Archer capsule, & an inflow of monocytes. Rapid growing & fibrosis of crescents compresses a hairlike loops & lessens a Archer space which leads to kidney failure inside weeks or even months.

Mesangial proliferative GN
This nature and severity is due to deposition of polymerised IgA1 in the mesangium, with the localised proliferation of tissue. These are uniform by using IgA nephritis (Berger's disease) and ordinarily presents by owning macroscopical haematuria.

Minimal change GN
This form of GN normally (though non alone) presents within youngsters by using nephrotic syndrome and massive proteinuria. These are controlled by owning steroids. When a title indicates, no changes in lightly microscopy.

Chronic glomerulonephritis
Chronic glomerulonephritis is a prevent-stage of completely glomerulonephritis sustaining unfavourable evolution.

Histopathology: couple glomeruli will however present changes which permit to discern a etiology of CGN. A majority of the glomeruli come affected. Based on the stage of the disease, it might present different degrees of hyalinisation (hyalinosclerosis - aggregate replacement of glomeruli & Archer's space using hyalin). A hyalin is an amorphous lesson, pink, homogeneous, resulted from either combination of plasma proteins, increased mesangial matrix & collagen. Altogether hyalin glomeruli come atrophic (little), lacking capillaries, hence non-functional. Obstruction of blood flow may make secondary cannular atrophy, interstitial fibrosis & thickening of the arterial wall by hyaloid deposits. Functional uriniferous tubule use dilated tubules, typically by using hyaloid casts in the lumens. In the interstitium is present an abundant inflammatory infiltrate (mostly sustaining lymph cell).

This general (glomerular, vascular & interstitial) warmness is a then-supposed "end stage kidney". Around virtually all subjects, these are associated using systemic high blood pressure.