Pediatric Rheumatology Online Journal → July 2003 → Childhood Lupus→ Case Reports → Abstract #112

TREATMENT QUANDARY: PROLIFERATIVE GLOMERULONEPHRITIS - LUPUS VERSUS HEPATITIS B INFECTION

E. M. Morgan DeWitt,¹ R. Q. Cron,¹ T. H. Finkel,¹ K. Meyers.²

¹Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA; ²Nephrology, Children's Hospital of Philadelphia, Philadelphia, PA

INTRODUCTION: The glomerulonephritis (GN) associated with Hepatitis B virus (HBV) infection can be morphologically similar to that caused by Systemic Lupus Erythematosus (SLE). Patients with SLE and coexistent HBV have milder manifestations of SLE than those without chronic HBV. We report a case of a patient who presented with GN and has both HBV and SLE.
CASE REPORT: 12 year old previously healthy African American male presented to the Emergency Department with 6 weeks of swelling, abdominal pain and fatigue. On admission he was hypertensive, had diffuse lymphadenopathy, edema, pleural effusions and ascites. Presenting lab findings were serum creatinine 2.5 mg/dl, albumin 1.4 mg/dl, ESR 80mm/hr, normal complement levels C3 139 mg/dl (90-187), C4 32.9mg/dl (16-45), normal liver enzymes ALT 21 U/L(10-55), AST 29 U/L(15-40). He underwent emergent renal biopsy prior to initiation of therapy which by light microscopy showed 100% crescentic, proliferative GN, with immunofluorescence positive for IgG, IgM, IgA, C1q and C3 ('full house'). He was treated with IV cyclophosphamide, pulsed methylprednisolone, and plasmapheresis. Lab results were subsequently positive for HBsAg, HBeAg, HB core Ab, with circulating viral load 200 million copies. The ANA was positive at a titer of 1:320, speckled pattern, dsDNA 255, Coombs+; these labs plus serositis and GN met criteria for SLE.
COMMENT: Whether or not the GN was due to SLE or HBV dictates the treatment regimen. Our concern was that high dose steroids could exacerbate the HBV, while interferon alpha could exacerbate the SLE. However, immunohistochemistry of the glomeruli for HBsAg was negative, and the 'full house' immunostaining in the setting of proliferative crescentic (not membranous) GN was consistent with SLE GN. The current treatment regimen is oral steroids, hydroxychloroquine and antihypertensives. The patient is doing well with minimal proteinuria, a serum creatinine of 1.4 mg/dl, and albumin 3.9 mg/dl. He is to start an antiretroviral to treat the active HBV infection.