A total of 163 Japanese children (90 boys and 73 girls, ranging in age from 3 to 15) with proteinuria and/or hematuria were studied for renal histopathology using biopsy materials by light microscopy, electron microscopy, and immunofluolescence method. Eleven patients were diagnosed as membranous nephropathy (MN) while the other 152 patients had various renal diseases other than MN. All patients with MN did not have any known predisposing of associated caused. Hepatitis B virus surface antigen (HBsAg) in the serum, as determined by a reversed passive hemagglutination method (RPHA), was positive in 100% of the patients with MN, while it was positive in 4.6% of the patients with other renal diseases. The difference was statistically significant. Of the 11 mothers of the children with MN, six were positive for HBsAg, and one of the remaining 2 was positive for antibody to HGsAg (anti-HBs) and another was not examined. These findings suggest that MN among Japanese children are mainly, if not exclusively, caused by hepatitis B virus (HBV) and that the virus is transmitted from the mother to child in most instances. In each case of HBsAg-associated glomerulonephritis reported, HBsAg was detected, by immunofluorescence, in the glomeruli, with a distribution similar to that of immunoglobulins. However deposits of HBsAg could not be demonstrated in the glomeruli of the 9 patients with MN studied. Pathogenic immune complexes in the glomerular lesions with subepithelial deposits have been shown to weigh less than 1 million daltons. Since the intact 20-nm HBsAg has a molecular weight of more than 2.4 million daltons, probably most immune complexes containing it would be very large and rapidly cleared by the reticuloendothelial system. Therefore, this failure to detect glomerular staining with anti-HBs antiserum may mean that MN is caused by some other antigen, of a lower molecular weight, associated with HBV, but not necessarily by HB surface antigen.