BACKGROUND: We encountered two cases of Chinese herb-induced Fanconi syndrome in Japan. One component of the chinese medicine was "Kan-mokutsu" (Aristolochia manshuriensis) in which aristolochic acids (AAs) were detected. METHODS: Renal biopsy showed flattening of proximal tubular epithelial cells and paucicellular interstitial fibrosis without glomerular lesions, all of which were in accordance with Chinese herb nephropathy (CHN). To date, many cases of CHN have been reported mainly as progressive renal failure in western countries. RESULTS: However, our cases were different from those in that they presented Fanconi syndrome. The detected AAs in our cases consisted of aristolochic acid (AA)-I, II and D. In contrast, in Belgium, the incriminated agent was Aristolochia fangchi which consisted of AA-I, B, C, and aristolactum. CONCLUSION: These findings could indicate that different components of AAs could cause different clinical lesions, or that the amount of ingested AAs might reflect clinical pictures, that is to say, our patients took lower volume of Chinese herbs and might be in an early stage of CHN. Furthermore, it is likely that susceptibility to this substance may be different among races. CHN would include two clinical aspects: subacute renal failure and adult-onset Fanconi syndrome. It is important to bear in mind that CHN could present Fanconi syndrome.
BACKGROUND: We encountered two cases of Chinese herb-induced Fanconi syndrome in Japan. One component of the chinese medicine was "Kan-mokutsu" (Aristolochia manshuriensis) in which aristolochic acids (AAs) were detected. METHODS: Renal biopsy showed flattening of proximal tubular epithelial cells and paucicellular interstitial fibrosis without glomerular lesions, all of which were in accordance with Chinese herb nephropathy (CHN). To date, many cases of CHN have been reported mainly as progressive renal failure in western countries. RESULTS: However, our cases were different from those in that they presented Fanconi syndrome. The detected AAs in our cases consisted of aristolochic acid (AA)-I, II and D. In contrast, in Belgium, the incriminated agent was Aristolochia fangchi which consisted of AA-I, B, C, and aristolactum. CONCLUSION: These findings could indicate that different components of AAs could cause different clinical lesions, or that the amount of ingested AAs might reflect clinical pictures, that is to say, our patients took lower volume of Chinese herbs and might be in an early stage of CHN. Furthermore, it is likely that susceptibility to this substance may be different among races. CHN would include two clinical aspects: subacute renal failure and adult-onset Fanconi syndrome. It is important to bear in mind that CHN could present Fanconi syndrome.