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Amyloidosis in chronic inflammatory disease

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2 min synopsisUK scopeSources checked 27 Aug 2026Clinical review pending
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Acute nephrotic or renal deterioration

New severe oedema, oliguria, pulmonary oedema, acute kidney injury, symptomatic hypotension, sepsis or venous thromboembolism in a patient with AA amyloidosis may represent nephrotic complication, infection, drug toxicity, renal-vein thrombosis or uncontrolled inflammatory disease rather than slow progression.

Action: Arrange same-day renal and acute assessment, measure kidney function, potassium, albumin, urine protein and infection and thrombosis markers, support oxygenation and volume carefully, stop nephrotoxins, investigate a precipitant and involve the inflammatory-disease and amyloidosis teams so acute care and precursor suppression continue together.

Synopsis

Detect AA amyloidosis in chronic inflammatory disease, confirm and type deposits rather than assuming their precursor, suppress serum amyloid A production through cause-specific control, and protect kidney and systemic function through coordinated specialist care.

  • AA amyloidosis is a complication of prolonged serum amyloid A elevation from inflammatory, autoinflammatory or infectious disease; it is not interchangeable with AL amyloidosis.
  • The common presentation is increasing albuminuria or proteinuria, nephrotic syndrome and progressive kidney impairment in someone with years of inflammatory burden.
  • First-line detection is urine ACR or PCR, albumin, creatinine and eGFR plus inflammatory activity and serum amyloid A where available; normal symptoms do not ensure low SAA.

Key red flags

Breathlessness, hypoxaemia, rapidly increasing oedema, oliguria or severe hypertension requires urgent evaluation for pulmonary oedema, acute kidney injury and nephrotic fluid complications.

Nephrotic emergency

Sudden dyspnoea, limb swelling, flank pain, oliguria, infection or hypotension can signal thrombosis, pulmonary oedema, sepsis or acute kidney injury.

Investigation priorities

01
Urine ACR or PCR and renal profileFirst step

Detect and stage renal involvement.

Management branches

Diagnostic sequenceConfirm deposits, type them, then identify the source

Persistent proteinuria, nephrotic syndrome or organ dysfunction occurs with chronic inflammation.

  1. Quantify urine protein and renal function, measure inflammatory activity and screen urgently for nephrotic complications and atypical urine sediment.
  2. Perform serum and urine immunofixation and free light chains, then obtain the safest informative Congo-red-positive tissue for expert fibril typing.
First-line disease modificationSuppress serum amyloid A continuously

AA type is confirmed and the precursor source is identifiable.

Key medicines

ColchicineFor adult FMF use 1–1.5 mg orally daily initially, once or divided; increase by 0.5 mg steps according to attacks and SAA to a maximum 3 mg daily if tolerated and specialist supervised.
CanakinumabFor an adult weighing at least 40 kg, give 150 mg subcutaneously every four weeks; if response is inadequate, specialist product guidance permits 300 mg every four weeks.
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Sources and review status6 sources · checked 27 Aug 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

Authoring stateRapid draftClinical stateAwaiting reviewJurisdictionUnited Kingdom