The association between hepatitis B virus (HBV) infection and the development of nephropathy remains controversial. The chronic carrier state of Hepatitis B Virus leads to the development of glomerulonephropathy, the commonest histological type being membranous nephropathy (MN), particularly in children. Other types of glomerulonephritis associated with HBV infection are less common. Spontaneous clearance of HBV antigens, particularly the HBeAg, leads to resolution of proteinuria. The isolation of immune complexes in the kidney suggests that the pathogenesis of the disease may have an immune-complex basis. Genetic studies suggest a possible genetic predisposition to the development of HBV-MN. Cellular immune mechanism studies suggest HBV-MN children seem to have an inadequate cellular immune response to HBcAg. Membranous nephropathy in patients with chronic HBV carriage is the result of an interaction of virus and host factors. Although the natural history of the disease suggests a tendency to remission with supportive therapy, there is considerable morbidity. Anti-viral therapy (interferon or lamivudine) accelerates clearance of the virus and proteinuria. Immunisation with HBV vaccination is the most effective tool to reduce the incidence of HBV-MN.