The efficacy of interferon (IFN) in the treatment of hepatitis B virus (HBV)-associated nephropathy in black children has not been established. Twenty-four black children with biopsy-proven HBV-associated nephropathy were recruited into the study during the period April 1997 to June 1999. Five defaulted treatment and were excluded from the primary analysis. IFNalpha 2b was administered for 16 weeks. Response to treatment was defined as loss of HBeAg, decrease in proteinuria, and prevention of deterioration in renal and liver function. A control group of 20 patients was followed up for the same period. Ten (52.6%) of the treated children responded with clearance of HBeAg by 40 weeks. None cleared HBsAg. All responders showed remission of proteinuria, 90% maintained normal renal function and 1 (10%) showed improvement of renal function. HBV DNA levels decreased in this group. Nine patients did not clear HBeAg; none showed remission of proteinuria, and two showed deterioration of renal function. Liver enzymes rose during treatment but subsequently declined irrespective of response to therapy. No serious side effects were encountered. Only 5% of controls showed spontaneous clearance of HBeAg, and none had remission of proteinuria. Black children with HBV-associated nephropathy show accelerated clearance of HBeAg with remission of proteinuria following treatment with IFNalpha 2b. IFNalpha 2b was well tolerated.

The nephrotic syndrome (NS) reported from Southern Africa is distinguished by unusual characteristics in African children and typical features among Indian children. A genetic basis for these differences is explored in 44 African and 33 Indian children with NS in this paper. HLA associations were detected in the 20 Indian children with minimal change NS (MCNS) and 12 African children with membranous NS. Previous studies of HLA antigens, which have all been performed on Caucasian children with MCNS or steroid-responsive NS (SRNS), have detected associations with HLAB and DR locus genes. In this report HLA Bw44, which is part of HLA B12, was found to be significantly more frequent in Indian children with MCNS or SRNS than in controls (45 and 12%, respectively, p < 0.04; relative risk 5.8). In contrast, African children with membranous nephropathy had a significantly increased frequency of HLA Bw21 (15% in patients and 1% in controls, p < 0.04; relative risk 22.1). HBsAg was positive in 9 of 11 patients tested in the latter group. We conclude that the interaction between heredity and environmental factors is central to the pathogenesis of membranous nephropathy and similar considerations may be important in the development of MCNS.

To our knowledge, this is the first report of HLA associations in black patients with HBVMN in whom Class 1 and 11 antigens were determined using molecular methodology. There was a high frequency of DQB1*0603 in subjects compared to controls, suggesting a possible genetic predisposition to the development of HBVMN.

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