In a healthy individual, the median plasma concentration of SAA is 3 mg per liter. This can increase to over 2000 mg per liter during an acute phase response and a sustained overproduction of SAA is required for the creation of the<unk>  deposits that define<unk> . High levels of SAA, however, is not a sufficient condition for the development of systemic<unk>  and it remains unclear what triggers the accumulation of<unk> . The<unk>  protein is mainly deposited in the liver, spleen and kidney, and<unk>  can lead to nephrotic syndrome and ESRD. Natural history studies show, however, that it is the kidney involvement that drives the progression of the disease. In general, old age, reduced serum albumin concentration, end stage kidney failure, and sustained elevated SAA concentration are all associated with poor prognosis.
AA amyloidosis
AL amyloidosis
Secondary systemic amyloidosis
Familial renal amyloidosis
Monoclonal gammopathy of undetermined significance
LECT2 amyloidosis
Organ-limited amyloidosis
Monoclonal gammopathy of renal significance