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Mesangial cell Mesangial matrix

Inflammatory injury (glomerulonephritis) is characterized by glomerular hypercellularity that


results from infiltrating hematopoietic cells (such as neutrophils and macrophages) and/or
proliferating glomerular cells. These effector cells induce other abnormalities, such as thrombosis,
necrosis, and crescent formation which, if extensive, can result in rapidly progressive
glomerulonephritis.

Noninflammatory lesions resulting from immune injury usually involve the glomerular podocyte
and are associated with a major functional change in the glomerulus that results in an increase in
glomerular permeability to albumin and other proteins.

Importance of the site of glomerular injury The major determinant of whether the patient
presents with glomerulonephritis and an active urine sediment or with proteinuria and little or no
hematuria is the site of glomerular injuryparticularly, which glomerular cells are involved.

There are three major types of intrinsic or resident glomerular cells: epithelial cells (visceral and parietal),
endothelial cells, and mesangial cells:

Glomerular visceral epithelial cells (podocytes) are separated from the circulation by the
glomerular basement membrane (GBM). Thus, glomerular injury primarily involving the podocytes is
commonly associated with little or no activation of circulating inflammatory cells. The net effect is
proteinuria, often associated with the nephrotic syndrome, with little or no hematuria and no red blood
cell casts.

Glomerular visceral epithelial cells can also contribute to crescent formation.

Glomerular parietal epithelial cells (PECs) cover the inner aspect of Bowman's capsule and
contribute to crescent formation.

Glomerular PECs can also contribute to replenishment of damaged podocytes.

In contrast to glomerular visceral and parietal epithelial cells, glomerular endothelial and mesangial
cells are not separated from circulating factors (eg, complement) or inflammatory cells (eg,
neutrophils, macrophages, and T cells). The net effect is glomerulonephritis with hematuria, possible
red blood cell casts, and varying degrees of proteinuria.

Other determinants of glomerular injury In addition to the site of glomerular injury, a number of other
factors can contribute to glomerular injury. These include:

The biologic properties of the immunoglobulins that form the deposits. As an example, complement-
fixing IgG subtypes(IgG1 and IgG3), cause more injury than immunoglobulins that activate
complement poorly, such(IgA and IgG4).

The mechanism by which the deposits are formed. Antigen-antibody interactions that take place
within the glomerulus (in situ immune complex formation) result in local complement activation and are
much more nephritogenic than passive trapping of similar complexes preformed in the circulation.

The amount of immune deposit formation. The greater the quantity of immune deposits, the greater
the degree of tissue injury.

Inflammatory Non-inflammatory
Complement (C5a for chemotaxis, T cell-derived factors
C5b-C9)
Neutrophils recruited by C5a Vasoactive agents
Macrophages (crescent and Cytokines
sclerosis)
Glomerular permeability factors
Complement C5b-9 (thicken GBM,
apoptosis of podocyte

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