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AA Amyloidosis Inflammatory Control Strategy — ESENeph MCQ

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HardGlomerulonephritisAA Amyloidosis Inflammatory Control StrategyESENeph

A 60-year-old man presents with bilateral lower limb oedema and proteinuria (uPCR 520 mg/mmol). Renal biopsy shows apple-green birefringence with Congo red. Mass spectrometry identifies AA amyloid. He has a 15-year history of poorly controlled rheumatoid arthritis. Serum amyloid A protein (SAA) is markedly elevated. What is the primary treatment strategy?

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Correct answer: C — Aggressive suppression of the underlying inflammatory disorder

AA amyloidosis is caused by chronic deposition of serum amyloid A protein (SAA) — an acute phase reactant produced during persistent inflammation. Unlike AL amyloidosis (which requires clone-directed chemotherapy), AA amyloidosis treatment centres on aggressive control of the underlying inflammatory condition. In rheumatoid arthritis, this means optimising disease-modifying therapy (biologics such as tocilizumab or anti-TNF agents) to suppress SAA production to <10 mg/L. Colchicine is specific for FMF-associated AA amyloidosis. Bortezomib targets plasma cell clones in AL amyloidosis. Organ function can stabilise or improve if SAA is suppressed.

Reference: Lachmann et al 2007 – AA Amyloidosis Outcomes; NICE 2023 – Amyloidosis Pathway