AA amyloidosis
protein deposition disease
AA amyloidosis is a form of amyloidosis, a disease characterized by the abnormal deposition of fibers of insoluble protein in the extracellular space of various tissues and organs. In AA amyloidosis, the deposited protein is serum amyloid A protein (SAA), an acute-phase protein which is normally soluble and whose plasma concentration is highest during inflammation.
Causes
AA amyloidosis is a complication of a number of inflammatory diseases and infections, although only a small portion of patients with these conditions will go on to develop AA amyloidosis. The most common presentation of AA amyloidosis is renal in nature, including proteinuria, nephrotic syndrome and progressive development of chronic kidney disease leading to end stage kidney disease (ESKD) and need for renal replacement therapy (e.g. dialysis or kidney transplantation). A natural history study of AA amyloidosis patients reported a number of conditions associated with AA amyloidosis:
Autoimmune diseases and inflammatory diseases
Adult-onset Still's disease
Ankylosing spondylitis
Behcet's disease
Crohn's disease and ulcerative colitis
Familial Mediterranean fever (FMF)
Giant cell arteritis
Gout
Hyper-IgD syndrome
Juvenile idiopathic arthritis
Muckle–Wells syndrome (MWS)
Neonatal-onset multisystem inflammatory disease
Psoriatic arthritis
Polyarteritis nodosa
Polymyalgia rheumatica
Rheumatoid arthritis
Sarcoidosis
Takayasu's arteritis
TNF receptor associated periodic syndrome
Chronic infections
Bronchiectasis
Chronic cutaneous ulcers
Chronic osteomyelitis
Chronic pyelonephritis
Hepatitis B
Leprosy
Tuberculosis
Whipple's disease
Cancer
Acute myeloid leukaemia
Adenocarcinoma of the gut
Basal cell carcinoma of the skin
Castleman's disease
Chronic myeloid leukaemia
Chronic lymphoid leukaemia
Follicular dendritic cell sarcoma
Gastrointestinal stromal tumours
Hairy cell leukaemia
Hepatic adenoma
Hodgkin's lymphoma
Mesothelioma
Non-Hodgkin lymphoma
Non-small-cell lung cancer
Ovarian carcinoma
Papillary bladder carcinoma
Pleomorphic splenic sarcoma
Renal cell carcinoma
Small cell carcinoma of the bladder
Uterine leiomyosarcoma
Waldenstrom's macroglobulinaemia
Chronic foreign body reaction
Silicone-induced granulomatous reaction
Immunodeficiencies
Common variable immunodeficiency
Cyclic neutropenia
HIV/AIDS
Hypogammaglobulinaemia
X-linked agammaglobulinaemia
Other conditions predisposing to chronic infections
Cystic fibrosis
Epidermolysis bullosa
IV drug use
Jejuno-ileal bypass
Paraplegia
Obesity
SAPHO syndrome
Schnitzler syndrome
Symptoms
Signs and symptoms of amyloidosis can vary depending on the affected organ. AA amyloidosis commonly affects kidneys, liver, and stomach.
Pathology
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 AA deposits that define AA amyloidosis. High levels of SAA, however, is not a sufficient condition for the development of systemic AA amyloidosis and it remains unclear what triggers the accumulation of AA.
The AA protein is mainly deposited in the liver, spleen and kidney, and AA amyloidosis 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.
The public source identifies “AA amyloidosis” as protein deposition disease. This brief keeps that definition visible, then builds a research path around amyloidosis, protein and deposition.
Why this record matters
A short description can identify a subject without explaining its stakes. For “AA amyloidosis”, the useful work is to connect “protein deposition disease” to the records capable of establishing context and consequence.
Named sources, stable identifiers and responsible institutions provide the strongest route from overview to verifiable evidence. The source revision retrieved here is dated Sep 1, 2026. The linked authority identifier is Q2844591. None of the 0 selected statements returned an explicit reference. The first chronological checks are 2000.
Overview language is designed for orientation and should not be treated as a substitute for the evidence cited beneath it. The source lead contains qualifying language; that uncertainty should survive quotation, summary and reuse. Authority statements aid reconciliation but still require their own references, qualifiers and ranks to be checked.
How to read it
Use the entry as an orientation point, then follow its citations and revision history. Names, dates and institutional relationships should be checked against the original record.
- Subject orientation
- Search vocabulary
- Locating named sources
The closest primary source, responsible institution and strongest cited specialist reference.
Three-step research path
- Establish the record: confirm the title “AA amyloidosis”, its source revision and the description used here.
- Expand the search: follow AA amyloidosis primary sources, AA amyloidosis archive and amyloidosis research across catalogues and specialist indexes.
- Test the account: compare the strongest cited source with the responsible institution’s current record and note any disagreement.
Questions for further research
- Which source most directly establishes the central claim about “AA amyloidosis”?
- What terminology or title could unlock a more precise catalogue search?
- Which institution is responsible for the underlying evidence?
Search terms from this dossier
This entry incorporates text from “AA amyloidosis” on English Wikipedia. Contributors are listed in the page history. Text is available under the Creative Commons Attribution-ShareAlike 4.0 License. Selected authority identifiers and statements are retrieved from Wikidata under CC0; their references and qualifiers remain part of the verification path.