Renal Digest
Electron microscopy
Clinical differential diagnosis
Pathologic differential diagnosis
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    Postinfectious glomerulonephritis, acute diffuse proliferative
     Key features:
Clinical: Occurs after acute, usually bacterial (commonly streptococcal) infection
Light microscopy: An acute diffuse proliferative pattern of glomerular injury, with neutrophilic infiltration of all glomeruli and prominent endocapillary proliferation
Immunofluorescence: Coarse granular deposition of C3, with or without immunoglobulin (commonly IgG) reactivity
Electron microscopy: “Hump”-like subepithelial, as well as subendothelial and mesangial electron-dense deposits

Postinfectious glomerulonephritis is an immune complex-mediated renal disease occurring after acute, usually bacterial (commonly streptococcal) infection. It can present with various patterns of glomerular injury, depending on the stage of disease progression. In acute phase, there is acute diffuse proliferative pattern; as the renal damage resolves, mesangioproliferative, sclerosing, or other patterns of injury may be seen.
Most authors consider acute postinfectious glomerulonephritis an entity associated with previous bacterial infection; immune complex diseases associated with persistent antigenemia seen in chronic viral, bacterial, and parasitic infections are considered to be “infectious” rather than “postinfectious” and are frequently associated with a membranoproliferative pattern of injury.

Post-streptococcal glomerulonephritis

Differential diagnosis:
Lupus nephritis, focal (class III)
Membranoproliferative glomerulonephritis (MPGN), idiopathic, type I
Immunoglobulin A (IgA) nephropathy, proliferative type

Occurs about three weeks after pharyngitis or acute skin infection
The most common causes are streptococci and other bacteria (staphylococci).
Pathogenesis: Most likely, bacterial antigens are deposited in the glomeruli, followed by formation of antibodies and in situ immune complexes with complement activation; there is some evidence of complement activation without the immunoglobulins in the presence of bacterial molecules as well.

Gross or microscopic hematuria, proteinuria, renal failure sometimes with oliguria
Rising ASO-titer in patients with post-streptococcal GN
Edema and hypertension
Rarely presents with rapidly progressive glomeruonephritis

Acute proliferative glomerulonephritis with numerous neutrophils and endocapillary hypercellularity in all or most glomeruli
Cellular crescents are frequently seen in isolated glomeruli; true crescentic form (involvement of 50% or more of glomeruli with crescents) is very unusual.
Fibrinoid necrosis and thrombosis are uncommon.
The tubulointerstitium may be unremarkable or show active inflammation with or without edema.


      In acute phase, there is strong coarse granular C3 reactivity, with usually less intense immunoglobulin (most commonly IgG) deposition. Lack of significant immunoglobulin reactivity may be seen in many cases. Three patterns of immunofluorescence reactivity have been described: starry sky (discrete random granules), garland (confluent subepithelial granular and band-like deposits), and mesangial pattern (usually during resolving phase).
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Electron microscopy:  
Visceral epithelial cells: Different degrees of injury and degenerative changes; the effacement of foot processes is usually focal, but sometimes extensive
Glomerular basement membranes: May show irregularities in thickness. Subepithelial “hump”-like deposits are characteristic of postinfectious GN; they may be sometimes large and confluent. “Spike” formation is not characteristic of this entity. Sometimes large subendothelial deposits and an intraluminal increase in inflammatory cells may be seen as well
Glomerular endothelial cells: May show non-specific signs of injury and reactive changes; tubuloreticular structures are not seen
Mesangium: Increase in cellularity and extracellular matrix, with sometimes large and confluent fine granular electron-dense deposits

Clinical differential diagnosis:  
MPGN (types I, II, III)
IgA nephropathy
Lupus nephritis
Rapidly progressive GN

Pathologic differential diagnosis:  
Proliferative lupus nephritis
IgA nephropathy
MPGN types I, II, III
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Acute diffuse proliferative postinfectious glomerulonephritis. Diffuse global hypercellularity due to infiltration of lymphocytes and neutrophils; H&E, 200x
Extensive hypercellularity due to a presence of mixed inflammatory infiltrate (lymphocytes and many neutrophils)
Cellular crescent and endocapillary proliferation
Intense interstitial inflammation and glomerular hypercellularity, H&E, 200x
Global glomerular hypercellularity (mesangial and endocapillary) and periglomerular interstitial inflammatory infiltrate
Aggresive form of postinfectious GN, with extracapillary (crescents) and endocapillary proliferative changes and marked interstitial inflammation
Cellular crescent and endocapillary proliferation
Numerous inflammatory cells within the capillary loop
Large subepithelial `hump`-like electron dense deposit
`Hump`-like subepithelial electron dense deposit
Subepithelial `hump`-like electron dense deposit. Note complete effacement of foot processes overlying the deposit
Coarse granular staining for C3 predominantly along the capillary loops
Coarse granular staining for IgG predominantly along the capillary loops
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