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Multiple recurrences of anti-glomerular basement membrane disease with variable antibody detection: can the laboratory be trusted?

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ABSTRACT

Anti-glomerular basement membrane (GBM) disease is commonly a monophasic illness. We present the case of multiple recurrences of anti-GBM disease with varying serum anti-GBM antibody findings. A 33-year-old female tobacco user presenting with hematuria was diagnosed with anti-GBM disease by renal biopsy. Five years later, she presented with alveolar hemorrhage and positive anti-GBM antibody. She presented a third time with alveolar hemorrhage but undetectable anti-GBM antibody. With each occurrence, symptoms resolved with plasmapheresis, intravenous methylprednisone and oral cyclophosphamide. The relationship between anti-GBM antibody findings and disease presentation is complex. Clinicians should be aware of the possibility of seronegative anti-GBM disease.

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Chest CT without IV contrast during admission in 2006 revealed diffuse patchy bilateral ground glass opacities, which along with lab evidence of anemia, is consistent with alveolar hemorrhage.
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SFW038F1: Chest CT without IV contrast during admission in 2006 revealed diffuse patchy bilateral ground glass opacities, which along with lab evidence of anemia, is consistent with alveolar hemorrhage.

Mentions: In 2006, 5 years after initial diagnosis, she presented with dyspnea, hemoptysis and gross hematuria. Hemoglobin was 8.5 g/dL and serum creatinine was 0.8 mg/dL. A chest x-ray and computed tomography (CT) were obtained and showed evidence of diffuse alveolar filling consistent with alveolar hemorrhage (Figure 1). Urine analysis was significant for moderate hemoglobin. Serum anti-GBM antibody was 112 AU/mL and serum ANCA was negative. Renal biopsy was not performed but she was treated for a presumed relapse of anti-GBM disease with plasmapheresis for 7 days, methylprednisone 1 g intravenously (IV) daily for three doses followed by 40 mg oral prednisone for 2 months and 2 mg/kg/day cyclophosphamide. She remained on the 2 mg/kg/day cyclophosphamide for 32 months prior to being tapered and discontinued due to loss of follow-up to care. At the end of a 7-day plasmapheresis treatment, anti-GBM antibody levels had returned to 0 UA/mL. During this relapse, she was hospitalized for 5 days and required intensive care unit (ICU) monitoring for 2 days due to hypotension and need for plasmapheresis. The hypotension resolved with two units of packed red blood cells and volume resuscitation. She required 4 L of supplemental oxygen on admission, but prior to discharge she showed no significant desaturations during a 6-min walk test.Fig. 1.


Multiple recurrences of anti-glomerular basement membrane disease with variable antibody detection: can the laboratory be trusted?
Chest CT without IV contrast during admission in 2006 revealed diffuse patchy bilateral ground glass opacities, which along with lab evidence of anemia, is consistent with alveolar hemorrhage.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5036896&req=5

SFW038F1: Chest CT without IV contrast during admission in 2006 revealed diffuse patchy bilateral ground glass opacities, which along with lab evidence of anemia, is consistent with alveolar hemorrhage.
Mentions: In 2006, 5 years after initial diagnosis, she presented with dyspnea, hemoptysis and gross hematuria. Hemoglobin was 8.5 g/dL and serum creatinine was 0.8 mg/dL. A chest x-ray and computed tomography (CT) were obtained and showed evidence of diffuse alveolar filling consistent with alveolar hemorrhage (Figure 1). Urine analysis was significant for moderate hemoglobin. Serum anti-GBM antibody was 112 AU/mL and serum ANCA was negative. Renal biopsy was not performed but she was treated for a presumed relapse of anti-GBM disease with plasmapheresis for 7 days, methylprednisone 1 g intravenously (IV) daily for three doses followed by 40 mg oral prednisone for 2 months and 2 mg/kg/day cyclophosphamide. She remained on the 2 mg/kg/day cyclophosphamide for 32 months prior to being tapered and discontinued due to loss of follow-up to care. At the end of a 7-day plasmapheresis treatment, anti-GBM antibody levels had returned to 0 UA/mL. During this relapse, she was hospitalized for 5 days and required intensive care unit (ICU) monitoring for 2 days due to hypotension and need for plasmapheresis. The hypotension resolved with two units of packed red blood cells and volume resuscitation. She required 4 L of supplemental oxygen on admission, but prior to discharge she showed no significant desaturations during a 6-min walk test.Fig. 1.

View Article: PubMed Central - PubMed

ABSTRACT

Anti-glomerular basement membrane (GBM) disease is commonly a monophasic illness. We present the case of multiple recurrences of anti-GBM disease with varying serum anti-GBM antibody findings. A 33-year-old female tobacco user presenting with hematuria was diagnosed with anti-GBM disease by renal biopsy. Five years later, she presented with alveolar hemorrhage and positive anti-GBM antibody. She presented a third time with alveolar hemorrhage but undetectable anti-GBM antibody. With each occurrence, symptoms resolved with plasmapheresis, intravenous methylprednisone and oral cyclophosphamide. The relationship between anti-GBM antibody findings and disease presentation is complex. Clinicians should be aware of the possibility of seronegative anti-GBM disease.

No MeSH data available.


Related in: MedlinePlus