Hepatitis C-associated glomerulonephritis masquerading as Goodpasture’s syndrome

Abstract

Anti-glomerular basement membrane (GBM) autoantibodies are associated with Goodpasture’s syndrome, characterised by lung and kidney involvement. We report a case with clinical disease demonstrating discrepant anti-GBM antibody results between assay platforms. A 39-year-old male presented with an eight-week history of haemoptysis and acute renal impairment, on a background of active hepatitis C infection. Creatinine was 256 μmol/L with haemoproteinuria, hypocomplementaemia, and positive anti-GBM level (65 U/mL Phadia ELiA; reference range >10 U/mL) which was confirmed on repeat testing. Treatment for Goodpasture’s syndrome was initiated with plasma exchange (PLEX) and intravenous cyclophosphamide. However, renal biopsy performed in parallel to treatment did not demonstrate characteristic linear GBM binding on direct immunofluorescence. Findings were instead consistent with hepatitis C-associated glomerulonephritis. ANCA by immunofluorescence was negative. Anti-PR3, anti-MPO and anti-CCP tested retrospectively by Phadia ELiA methods were also positive, raising suspicion for an interfering factor. Pre-treatment sera tested for anti-GBM antibodies via indirect immunofluorescence (INOVA primate kidney) and chemiluminescence assay (INOVA BIO-FLASH) were negative. Unfortunately, pre-treatment cryoglobulins had not been tested. However, testing 6 months after presentation confirmed type 2 cryoglobulins, and anti-GBM levels had normalised. Cryoglobulins or another interfering factor may have caused platform-specific assay interference, affecting anti-GBM and other autoantibody detection on the same platform.