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  • Pathogenesis : abnormal proteinaceous deposits accumulate within tissues.
  • Signs : depend on which tissues are disrupted by amyloid accumulation.
  • May be systemic or localized: kidneys often affected , also liver and spleen.
  • Treatment : few options: colchicine and dimethyl sulfoxide (DMSO) have been tried.
  • Prognosis : usually progressive until death.
  • Familial and sporadic forms also occur.


Clinical signs

  • Dehydration.
  • Dyspnea (if pulmonary thrombosis).
  • Hindleg paralysis (if aortic thrombosis).

Differential diagnosis




  • Poor; usually progressive deposition. Fibrils are resistant to phagocytosis or proteolysis.

Expected response to treatment

  • Improvement in clinical signs.
  • Lack of progression of disease.

Reasons for treatment failure

  • Disease usually progressive.
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