It is understood that amyloidosis is the result of deposition of amyloid. Amyloid is an abnormal insoluble extracellular protein which may cause organ dysfunction and a wide variety of clinical syndromes. Amyloid deposition can disrupt the tissue structure of an involved organ and consequently leads to organ failure. Genetic mutations in different genes may lead to misfolded protein product. Genes involved in the pathogenesis of familial amyloidosis encode the culprit proteins, such as transthyretin, apolipoprotein AI, apolipoprotein AII, lysozyme, gelsolin, fibrinogen Aa-chain, and cystatin C.
Familial amyloidosis pathophysiology
Primary amyloidosis pathophysiology
Renal amyloidosis pathophysiology
POEMS syndrome pathophysiology
Primary amyloidosis other imaging findings
Familial amyloidosis risk factors
Secondary amyloidosis other imaging findings
Familial amyloidosis other imaging findings