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AA Amyloidosis — SCE Rheumatology MCQ

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HardRheumatoid ArthritisAA AmyloidosisSCE Rheumatology

A 55-year-old woman has a 12-year history of seropositive rheumatoid arthritis with persistent synovitis and raised inflammatory markers despite multiple DMARDs. She also has type 2 diabetes mellitus. She develops oedema, proteinuria of 5.8 g/day and a serum albumin concentration of 22 g/L. Serum immunofixation detects an IgG-kappa paraprotein of 4 g/L, with a normal serum free light-chain ratio. Renal biopsy shows glomerular and vascular amorphous deposits that stain with Congo red and demonstrate apple-green birefringence under polarised light. Laser-microdissection tandem mass spectrometry identifies SAA1- and SAA2-derived peptides as the amyloid fibril proteins, without immunoglobulin light-chain-derived fibril protein. What is the diagnosis?

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Correct answer: D — AA (secondary) amyloidosis

The diagnosis is AA (secondary) amyloidosis. Congo-red staining with apple-green birefringence establishes amyloid, while identification of SAA1/SAA2-derived fibril proteins definitively types it as AA. Persistently active rheumatoid arthritis provides sustained production of the acute-phase reactant serum amyloid A, and renal AA amyloidosis typically presents with heavy proteinuria and nephrotic syndrome. The small IgG-kappa paraprotein may represent MGUS and does not override direct tissue typing; AL amyloidosis requires a light-chain-derived fibril protein. Diabetic nephropathy, membranous nephropathy and minimal change disease do not produce Congo-red-positive deposits with this proteomic profile. Management centres on effective suppression of the underlying inflammation and serum amyloid A production; anti-SAP antibody therapy is not established routine treatment.

Reference: Mirioglu S, et al. AA Amyloidosis: A Contemporary View. Current Rheumatology Reports. 2024;26:248–259. https://pubmed.ncbi.nlm.nih.gov/36759076/