2427 A Case of Hepatitis B Virus-Related Membranous Nephropathy in an Adult With Low Hepatitis B Viral Load

Abstract

INTRODUCTION: Hepatitis B virus (HBV) infection is an important etiologic factor for secondary membranous nephropathy (MN), especially in regions with endemic HBV infection. Though an uncommon occurrence, it is crucial to recognize HBV-related MN as it may progress to renal failure in untreated adults. In patients with HBV infection, it is critical to exclude other secondary causes of MN. This case describes a case of HBV-related MN in a HBeAg-negative patient with low HBV viral load. CASE DESCRIPTION/METHODS: Mr C is a 64 year old gentleman who has underlying chronic HBV infection and Stage 3b chronic kidney disease. He presented with bilateral lower limb swelling. He was found to have hypoalbuminemia and nephrotic range proteinuria associated with microscopic hematuria. He was in “inactive chronic HBV carrier infection” phase with negative hepatitis B e antigen (HBeAg), positive anti-HBe and low HBV viral load 2.68 log IU/ml with positive antinuclear antibody and low complement C3. Other workup for secondary causes of membranous nephropathy was unyielding. Renal biopsy showed membranous nephropathy with focal proliferative glomerulonephritis. Immunofluorescence was not suggestive of lupus nephritis and staining for antiphospholipase A2 receptor was negative. He was diagnosed as HBV-related MN and he was treated with Tenofovir Alafenamide. Six months after HBV treatment, his proteinuria has improved with stable renal function. HBV viral load was suppressed to less than 1.3 log IU/ml but he still had high titer of HBsAg (7000 IU/ml) as expected. DISCUSSION: In HBV-related MN, HBV treatment is recommended as previous studies showed that HBV treatment and HBeAg clearance are associated with remission of MN. However, treatment endpoint remains unclear. The pathogenesis of HBV-related glomerular disease is due to the deposition of HBV antigens immune complexes in the glomerulus, especially to HBeAg. Therefore, MN can occur in patients with low HBV viral load. In HBeAg-positive patients, it may be reasonable to consider stopping antiviral following clearance of HBeAg. In HBeAg-negative patients, HBsAg immune complexes may contribute to MN. As in this case, it may be prudent to continue with HBV therapy as he has persistently high HBsAg titer. Future research is needed to find reliable HBV markers to guide management and define clinical end points for patients with HBV-related MN.