The initial symptoms are those of a tubulointerstitial nephritis of the sort met with after toxic aggressions to the proximal convoluted tubules. Such proximal tubule nephropathies can be induced by aluminium (e.g. in antiperspirants), antibiotics (vancomycin, aminosides), tenofovir (for AIDS), and cisplatin. Their symptoms are well known to nephrologists: glycosuria without hyperglycemia, microalbuminuria, poor urine concentration capacity, impaired urine acidification, and yet long-lasting normal creatinine clearance. In BEN, renal biopsy shows acellular interstitial fibrosis, tubular atrophy, and karyomegaly in proximal convoluted tubules. A number of descriptive studies have suggested a correlation between exposure to ochratoxin A and BEN, and have found a correlation between its geographical distribution and a high incidence of, and mortality from, urothelial urinary tract tumours. However, insufficient information is currently available to conclusively link ochratoxin A to BEN. The toxin may require synergistic interactions with predisposing genotypes or other environmental toxicants to induce this nephropathy. Ochratoxin possibly is not the cause of this nephropathy, and many authors are in favor of aristolochic acid, that is contained in a plant: birthwort ("Aristolochia clematitis"). Nevertheless, although many of the pieces of scientific evidence are lacking and/or need serious re-evaluation, it remains that ochratoxin, in pigs, demonstrates direct correlation between exposure and onset and progression of nephropathy. This porcine nephropathy bears typical signs of toxicity to proximal tubules: loss of ability to concentrate urine, glycosuria, and histological proximal tubule degeneration.