
Health Dictionary
Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.
Amyloidosis laboratory findings
Introduction
Overview
Overview
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
Laboratory Findings
Cardiac
- 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
- Liver function tests, including:
- AST
- ALT
- Total bilirubin
- Alkaline phosphatase
- Albumin
Renal
- 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
- Common tests that are abnormal in thyroidal involvement of amyloidosis include:
- TSH
- Free T4
Bone marrow
- 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
References
- ↑ 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.
- ↑ 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.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]; Associate Editor(s)-in-Chief: Shaghayegh Habibi, M.D.[3]
