Dear Sir,
Chinese herbs nephropathy (CHN), associated with the ingestion of herbal remedies containing aristolochic acid (AA), was first reported in young Belgian women who have been on a slimming regimen including the Chinese herb Aristolochia fangchi. 1 CHN is a unique rapidly progressive nephropathy characterized by extensive renal interstitial fibrosis, tubular proteinuria, early and severe anemia and a high risk of urothelial cancer. [2][3][4] AA is a mixture of structurally related nitrophenanthrene carboxylic acids with aristolochic acid I (AAI) being the major component. AA is nephrotoxic in several species, mutagenic in bacteria and carcinogenic in rodents. 1 The detection of specific AA-DNA adducts by 32 P-postlabeling in kidney and ureter tissue of CHN patients unambiguously demonstrated a causative role of AA in CHN. 4 -7 CHN and urothelial tumors have recently been reported in patients who were exposed to Aristolochia species and had no relationship with the Belgian slimming clinic. 8,9 These reports demonstrate that the development of CHN lesions may be ascribed to the toxicity of AA alone without requiring the other drugs prescribed in the slimming regimen. Moreover, the recent demonstration of renal interstitial fibrosis and urothelial malignancy in rabbits treated with AA alone, removed any doubt on the causal role of AA in CHN. 10 It has been proposed to designate the interstitial nephropathy in which the unequivocal role of AA has been fully documented as aristolochic acid nephropathy (AAN). 1,9 On both clinical and morphological grounds, AAN is very similar to another fibrosing nephropathy, the Balkan endemic nephropathy (BEN), which is found in certain rural areas of Rumania, Croatia, Bosnia, Serbia and Bulgaria along the Danube river basin. 2,11,12 Both diseases share normal blood pressure, aseptic leukocyturia, early and severe anemia on clinical ground and morphologically extensive hypocellular interstitial sclerosis, tubular atrophy, global sclerosis of glomeruli, cellular atypia and malignant transformation of the urothelium. 2- 4,11,12 These similarities have led to the hypothesis of a common etiological agent for both diseases. In this context it is noteworthy that food contamination by AA has been suggested as a possible causal factor in BEN in 1970. 13 Alternatively evidence has accumulated that BEN is an environmentally in-