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Abstract: PO1789

Hepatitis B-Associated Lupus-Like Nephritis

Session Information

Category: Trainee Case Report

  • 1202 Glomerular Diseases: Immunology and Inflammation


  • Vincent-Johnson, Anita, University of Virginia, Charlottesville, Virginia, United States
  • Al Mulhim, Mohammed Yousef, University of Virginia, Charlottesville, Virginia, United States
  • Cathro, Helen P., University of Virginia, Charlottesville, Virginia, United States
  • Chopra, Tushar, University of Virginia, Charlottesville, Virginia, United States
  • Pourafshar, Negiin, University of Virginia, Charlottesville, Virginia, United States

The spectrum of renal disease with hepatitis B virus (HBV) is broad including different glomerular lesions related to the presence of viral antigens. HBV-associated lupus-like nephritis (HBLN) is characterized by immune deposits of polyclonal immunoglobulins linked to polytypic complements in glomeruli, structures reminiscent of lupus nephritis (LN). There is a dearth of literature regarding differentiation of HBLN and LN along with differing management and outcomes.

Case Description

We report a 46-year-old male with known HBV infection with 3 weeks of progressive dyspnea and edema. The serum creatinine (SCr) rose from a baseline of 0.8 mg/dl to 5.2 mg/dl with proteinuria of 1.7 g/g and microscopic hematuria. Serology showed transiently positive ANA, negative anti ds-DNA, and low levels of C3. Hepatitis B e Ag and hepatitis B surface Ag were positive, and the viral load was 2483 IU/mL with normal liver enzymes. A renal biopsy revealed severe diffuse endocapillary hypercellularity, a “full house” immunofluorescent pattern, and numerous subendothelial and mesangial immune deposits ultrastrurally, findings consistent with a diagnosis of HBLN. The patient was started on Entecavir for treatment of hepatitis B. After 2 months of treatment, the Scr improved to 1.97 mg/dL with improvement in initial symptoms.


Our case highlights the inherent difficulty in recognition of renal failure secondary to HBLN with associated pathology findings consistent with LN in the presence of hepatitis B infection. Although the full-house immunofluorescent pattern generally implies a diagnosis of LN, renal biopsy findings have to be interpreted in the clinical context. All the findings in renal biopsies of LN can also be seen in HBLN. Renal manifestations in both groups, including proteinuria and Scr, can be similar. Although considerably lower C3 levels in patients with lupus may suggest more widespread extrarenal disease, low C3 levels have also been reported in HBLN. The distinguishing feature between HBLN and LN is the presence of HBeAg and hepatitis B DNA. Our case is an unusual presentation of hepatitis B with renal involvement with effective diagnosis and management. While there is limited data for the treatment of HBLN with most studies excluding patients with an elevated SCr, small studies suggest first-line treatment with antiviral agents to achieve viral clearance.