1. Schematic diagram of a lobe of a normal glomerulus.

2. Deposition of immune complexes as seen by immunofluorescence
Two patterns of deposition of immune complexes as seen by immunofluorescence microscopy. A, Granular, characteristic of circulating and in situ immune complex deposition. B, Linear, characteristic of classic anti-GBM antibody GN.

3. FSGS
High-power view of focal and segmental glomerulosclerosis (PAS stain), seen as a mass of scarred, obliterated capillary lumens with accumulations of matrix material, that has replaced a portion of the glomerulus.
This trichrome stain of a glomerulus in a patient with FSGS demonstrates blue collagen deposition. FSGS accounts for about a sixth of cases of nephrotic syndrome in adults and children.

4. Membranous nephropathy
A, Diffuse thickening of the glomerular basement membrane. B, Schematic diagram illustrating subepithelial deposits, effacement of foot processes, and the presence of "spikes" of basement membrane material between the immune deposits.

5. Membranous nephropathy
By electron microscopy in membranous glomerulonephritis, the darker electron dense sub-epithelial immune deposits are separated by an intervening small, spike-like protrusions of GBM

6. Membranous nephropathy
Membranous glomerulonephritis is an immunologically mediated disease in which peripheral and granular deposits of mainly IgG and complement collect in the basement membrane

7. Membranous nephropathy
A silver stain of the glomerulus highlights the proteinaceous basement membranes in black. There are characteristic "spikes" seen with membranous glomerulonephritis seen here in which the black basement membrane material appears as projections around the capillary loops.

8. Membranoproliferative GN
A, showing mesangial cell proliferation, basement membrane thickening, leukocyte infiltration, and accentuation of lobular architecture. B, Schematic representation of patterns in the two types of membranoproliferative GN. In type I there are subendothelial deposits; type II is characterized by intramembranous dense deposits (dense-deposit disease). In both, mesangial interposition gives the appearance of split basement membranes when viewed by light microscopy.

9. Acute diffuse post-streptococcal GN
A, Glomerular hypercellularity is caused by intracapillary leukocytes and proliferation of intrinsic glomerular cells. Note the red cell casts in the tubules. B, Typical electron-dense subepithelial "hump" (arrow) and intramembranous deposits. BM, basement membrane; CL, capillary lumen; E, endothelial cell; Ep, visceral epithelial cells (podocytes).

10. Acute postinfectious (Poststreptococcal) GN
The hypercellularity of post-streptococcal glomerulonephritis is due to increased numbers of epithelial, endothelial, and mesangial cells as well as neutrophils in and around the capillary loops. This disease may follow several weeks after infection with certain strains of group A beta hemolytic streptococci. Patients typically have an elevated anti-streptolysin O (ASO) titer.

11. Acute post-infectious (Poststreptococcal) GN
Post-streptococcal glomerulonephritis is immunologically mediated, and the immune deposits are distributed in the capillary loops in a granular, bumpy pattern because of the focal nature of the deposition process.

12. IgA nephropathy
A, Light microscopy showing mesangial proliferation and matrix increase.
B. There is characteristic immunofluorescence deposition of IgA, principally in mesangial regions.

13. Berger's disease (IgA nephropathy)
The IgA is deposited mainly in mesangium, which then increases mesangial cellularity as shown at the arrow.
This immunofluorescence micrograph demonstrates positivity with antibody to IgA. Note that the pattern is that of mesangial staining.

14. Crescentic GN (PAS stain)
Note the collapsed glomerular tufts and the crescent-shaped mass of proliferating cells and leukocytes internal to Bowman's capsule.

15. Causes of chronic GN d

16. Chronic GN
A Masson trichrome preparation shows complete replacement of virtually all glomeruli by blue-staining collagen.