Systemic Amyloidosis in Cats

Aetiology & Pathogenesis
Amyloidosis is potentially the result of a variety of disease processes which lead to the deposition of extracellular (intercellular) fibrillar protein material (amyloid). There are several different types of amyloid, but they have a similar appearance due to the physical conformation of the fibrils (a b-pleated sheet).
The pathogenesis of amyloidosis involves the excessive production of the amyloidogenic protein, and/or defective proteolysis, and/or a structural abnormality of the protein. In some species, some normal proteins are amyloidogenic (if present in sufficient concentrations will be deposited in tissues as amyloid) and disease may develop in association with excessive production of such proteins and/or reduced removal/proteolysis. Other cases of amyloidosis are associated with the production of abnormal proteins by cells or normal proteins that have an abnormal structure (eg, due to genetic defects) that renders them amyloidogenic. The b-pleated sheet configuration of amyloid is responsible for the insolubility of the fibrils, and its resistance to proteolysis. Although inert, the deposition of amyloid within organs can result in progressive interference with normal function and blood flow, and may result in necrosis and fibrosis.

Three types of systemic amyloidosis are recognised in humans:
• Immunoglobulin-related
• Reactive
• Heredo-familial

Immunoglobulin-related amyloidosis:
Immunoglobulin-related amyloidosis is where the amyloid protein is a degradation product of the light-chain from an immunoglobulin (eg, has been reported in association with multiple myeloma and paraproteinaemia). Immunoglobulin-related amyloidosis has been described in a variety of different species, including the cat (in association with IgG-related myeloma), but is rare. [...]