Goodpasture syndrome laboratory findings: Difference between revisions
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==Laboratory Findings== | ==Laboratory Findings== | ||
Laboratory findings consistent with the diagnosis of Goodpasture syndrome include presence of | Laboratory findings consistent with the diagnosis of Goodpasture syndrome include presence of [[autoantibodies]] such as [[Anti-glomerular basement membrane antibody|anti-glomerular basement membrane antibodies.]]<ref name="pmid16234289">{{cite journal |vauthors=Sinico RA, Radice A, Corace C, Sabadini E, Bollini B |title=Anti-glomerular basement membrane antibodies in the diagnosis of Goodpasture syndrome: a comparison of different assays |journal=Nephrol. Dial. Transplant. |volume=21 |issue=2 |pages=397–401 |date=February 2006 |pmid=16234289 |doi=10.1093/ndt/gfi230 |url=}}</ref><ref name="pmid19741587">{{cite journal |vauthors=Zhao J, Cui Z, Yang R, Jia XY, Zhang Y, Zhao MH |title=Anti-glomerular basement membrane autoantibodies against different target antigens are associated with disease severity |journal=Kidney Int. |volume=76 |issue=10 |pages=1108–15 |date=November 2009 |pmid=19741587 |doi=10.1038/ki.2009.348 |url=}}</ref><ref name="pmid19151145">{{cite journal |vauthors=Yang R, Hellmark T, Zhao J, Cui Z, Segelmark M, Zhao MH, Wang HY |title=Levels of epitope-specific autoantibodies correlate with renal damage in anti-GBM disease |journal=Nephrol. Dial. Transplant. |volume=24 |issue=6 |pages=1838–44 |date=June 2009 |pmid=19151145 |doi=10.1093/ndt/gfn761 |url=}}</ref> | ||
* Other findings associated with pulmonary and renal injury include elevated blood urea nitrogen, low-grade proteinuria, gross or microscopic hematuria, and red cell casts. | * 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 should be done to determine and rule out the presence of ANCA associated vasculitis.<ref name="pmid1317224">{{cite journal |vauthors=Weber MF, Andrassy K, Pullig O, Koderisch J, Netzer K |title=Antineutrophil-cytoplasmic antibodies and antiglomerular basement membrane antibodies in Goodpasture's syndrome and in Wegener's granulomatosis |journal=J. Am. Soc. Nephrol. |volume=2 |issue=7 |pages=1227–34 |date=January 1992 |pmid=1317224 |doi= |url=}}</ref> | * If laboratory test cannot detect the presence of [[Anti-glomerular basement membrane antibody|anti-glomerular basement membrane antibodies]], other tests such as [[Anti-neutrophil cytoplasmic antibody|anti-neutrophil cytoplasmic antibodies]] (ANCA) should be done to determine and rule out the presence of [[ANCA]] associated [[vasculitis]].<ref name="pmid1317224">{{cite journal |vauthors=Weber MF, Andrassy K, Pullig O, Koderisch J, Netzer K |title=Antineutrophil-cytoplasmic antibodies and antiglomerular basement membrane antibodies in Goodpasture's syndrome and in Wegener's granulomatosis |journal=J. Am. Soc. Nephrol. |volume=2 |issue=7 |pages=1227–34 |date=January 1992 |pmid=1317224 |doi= |url=}}</ref> | ||
* Routine laboratory test that may be ordered to help in identifying the cause are: | * Routine laboratory test that may be ordered to help in identifying the cause are: | ||
** Complete blood count (leukocytosis and anemia) | ** [[Complete blood count]] ([[leukocytosis]] and [[anemia]]) | ||
** Renal function test (BUN, S. creatinine ) | ** [[Renal function tests|Renal function test]] ([[Blood urea nitrogen|BUN]], [[Serum creatinine|S. creatinine]]) | ||
** Urinalysis for proteinuria, hematuria, and red cell casts | ** [[Urinalysis]] for [[proteinuria]], [[hematuria]], and red cell casts | ||
** ESR and CRP | ** [[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. | *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 lung disease|restrictive pattern]] on PFTs. | ||
*The diffusing capacity for carbon monoxide (DLCO) is also elevated due to destruction of alveolar basement membrane and subsequent fibrosis. | *The diffusing capacity for carbon monoxide ([[DLCO]]) is also elevated due to destruction of [[alveolar]] [[basement membrane]] and subsequent [[fibrosis]]. | ||
==References== | ==References== | ||
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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]
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 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
- ↑ 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.