
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.
Goodpasture syndrome laboratory findings
Introduction
Overview
Overview
Laboratory findings consistent with the diagnosis of Goodpasture syndrome include presence of autoantibodies such as anti-glomerular basement membrane antibodies. Other findings associated with pulmonary and renal injury include elevated blood urea nitrogen, low-grade proteinuria, gross or microscopic hematuria, and red cell casts.
Laboratory Findings
Laboratory Findings
Laboratory findings consistent with the diagnosis of Goodpasture syndrome include presence of autoantibodies such as anti-glomerular basement membrane antibodies.[1][2][3]
- Other findings associated with pulmonary and renal injury include elevated blood urea nitrogen, low-grade proteinuria, gross or microscopic hematuria, and red cell casts.
- If laboratory test cannot detect the presence of anti-glomerular basement membrane antibodies, other tests such as anti-neutrophil cytoplasmic antibodies (ANCA) should be done to determine and rule out the presence of ANCA associated vasculitis.[4]
- Routine laboratory test that may be ordered to help in identifying the cause are:
- Complete blood count (leukocytosis and anemia)
- Renal function test (BUN, S. creatinine)
- Urinalysis for proteinuria, hematuria, and red cell casts
- ESR and CRP
- Pulmonary function testing (PFT) may be done to determine the extent of disease as patients with Goodpasture syndrome tend to have interstitial fibrosis and a restrictive pattern on PFTs.
- The diffusing capacity for carbon monoxide (DLCO) is also elevated due to destruction of alveolar basement membrane and subsequent fibrosis.
References
References
- ↑ Sinico RA, Radice A, Corace C, Sabadini E, Bollini B (February 2006). “Anti-glomerular basement membrane antibodies in the diagnosis of Goodpasture syndrome: a comparison of different assays”. Nephrol. Dial. Transplant. 21 (2): 397–401. doi:10.1093/ndt/gfi230. PMID 16234289.
- ↑ Zhao J, Cui Z, Yang R, Jia XY, Zhang Y, Zhao MH (November 2009). “Anti-glomerular basement membrane autoantibodies against different target antigens are associated with disease severity”. Kidney Int. 76 (10): 1108–15. doi:10.1038/ki.2009.348. PMID 19741587.
- ↑ Yang R, Hellmark T, Zhao J, Cui Z, Segelmark M, Zhao MH, Wang HY (June 2009). “Levels of epitope-specific autoantibodies correlate with renal damage in anti-GBM disease”. Nephrol. Dial. Transplant. 24 (6): 1838–44. doi:10.1093/ndt/gfn761. PMID 19151145.
- ↑ Weber MF, Andrassy K, Pullig O, Koderisch J, Netzer K (January 1992). “Antineutrophil-cytoplasmic antibodies and antiglomerular basement membrane antibodies in Goodpasture’s syndrome and in Wegener’s granulomatosis”. J. Am. Soc. Nephrol. 2 (7): 1227–34. PMID 1317224.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Ali Poyan Mehr, M.D. [2]; Associate Editor(s)-in-Chief: Krzysztof Wierzbicki M.D. [3] Akshun Kalia M.B.B.S.[4]
