Trace the biochemistry. Sustained inflammation drives hepatic synthesis of the acute-phase protein serum amyloid A ($SAA$), a high-density-lipoprotein-associated apolipoprotein. When inflammation is chronic and unresolved, $SAA$ is cleaved and its insoluble fragments aggregate into beta-pleated fibrils - this deposited material is termed $AA$ amyloid, and the resulting disease is reactive (secondary) systemic amyloidosis.
Rheumatoid arthritis is the prototypical Western cause; worldwide, chronic infections such as tuberculosis and osteomyelitis contribute heavily. The kidney is the dominant target organ, explaining the heavy proteinuria.
The alternatives map to different precursors: light-chain $AL$ to plasma-cell dyscrasias, $A\beta_2$-microglobulin to chronic dialysis, and transthyretin $ATTR$ to senile/hereditary cardiac amyloidosis.
\[\boxed{\text{Chronic inflammation} \rightarrow SAA \rightarrow AA\ \text{amyloid}}\]