Pathogenesis of glomerular disease

1. Immune-complex mediated GN (glomerulonephritis):

Capillary is the perfect trap from immune complexes (IC), which may be floating around in plasma. This deposition of IC is bad enough. What’s even worse is that these IC activate complement. Activated complement (i.e., C5a) is chemotactic, so it attracts other inflammatory cells to the area, which are likely to cause a lot of damage. These complexes can also activate mesangial cells to secrete mesangial matrix and other substances, which can cause damage.

IF (immunofluorecence): granular deposition.

Antigens can be:

Exogenous: ex: post-sterptococcal GNs

Endogenous: SLE (anti-DNA)

2. Antibodies to BM in the glomerulus:

Ex: Goodpasteur’s.

IF: linear deposition.

3. Associated with ANCA (Antibodies against cytoplasmic elements in PMNs)

As a result, these antibodies bind to PMNs, making them more ”sticky,” thus enabling them to adhere to capillaries in the glomerulus. Ex: Wegner’s granulomatosis.

Category: Nephrology Notes , Pathology Notes