Amyloidosis laboratory findings

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]; Associate Editor(s)-in-Chief:  Shaghayegh Habibi, M.D.[3]

## Overview[edit | edit source]

Laboratory findings in amyloidosis include elevated erythrocyte sedimentation rate, increased BUN level, serum creatinine, protein, casts, or fat bodies in urine. Serum troponin, B-type natriuretic peptide, and beta-2-microglobulin are prognostic markers for heart failure. Amyloid deposits can be identified histologically by Congo red staining and viewing under polarized light where amyloid deposits produce a distinctive 'apple green birefringence'. Alternatively, thioflavin T stain may be used. An abdominal fat pad aspiration, rectal mucosa biopsy, or bone marrow biopsy can help confirm the diagnosis. They reveal positive findings in 80% patients.

## Laboratory Findings[edit | edit source]

### Cardiac[edit | edit source]

* Cardiac biomarkers are the most important predictors of outcome in amyloidosis.
* They provide a quantitative assessment for cardiac damage and wall strain.[1]
* The biomarkers include:

* Troponin I or Troponin T
* BNP and NT-proBNP

### Hepatic[edit | edit source]

* Liver function tests, including:

* AST
* ALT
* Total bilirubin
* Alkaline phosphatase
* Albumin

### Renal[edit | edit source]

* A variety of kidney function tests can suggest amyloidosis.
* These tests include abnormalities in:

* Serum creatinine
* Urinary protein
* Glomerular filtration rate
* Albumin to creatinine ratio in the urine

### Thyroid[edit | edit source]

* Common tests that are abnormal in thyroidal involvement of amyloidosis include:

* TSH
* Free T4

### Bone marrow[edit | edit source]

* Concurrent multiple myeloma can be found in patients with amyloidosis.
* In such cases, laboratory testing should include[2]:

* Serum protein electrophoresis
* Immunoglobulin levels
* Serum free light chains
* Beta-2-microglobulin

## References[edit | edit source]

1. ↑ Merlini G, Seldin DC, Gertz MA (May 2011). "Amyloidosis: pathogenesis and new therapeutic options". J. Clin. Oncol. 29 (14): 1924–33. doi:10.1200/JCO.2010.32.2271. PMC 3138545. PMID 21483018.
2. ↑ Kourelis TV, Kumar SK, Gertz MA, Lacy MQ, Buadi FK, Hayman SR; et al. (2013). "Coexistent multiple myeloma or increased bone marrow plasma cells define equally high-risk populations in patients with immunoglobulin light chain amyloidosis". J Clin Oncol. 31 (34): 4319–24. doi:10.1200/JCO.2013.50.8499. PMC 4881366. PMID 24145344.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)

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