Ochratoxin A (OA) derives its name from Aspergillus ochraceus, the first mold from which it was isolated. It is the main toxic component in cultures of this mold.1 Related fungal metabolites are the methyl and ethyl esters of OA, and the dechloro derivative ochratoxin B and its esters.2, 3 These were not discovered as a result of investigations into the etiology of a disease, but as a result of large-scale toxicity screening of molds present in South African foods.4 Such screening has yielded numerous new compounds referred to as mycotoxins, but the link between these toxins and animal or human disease has remained tenuous in many cases. In contrast, the significance of OA as an agent of disease soon became evident. Following its discovery in 1965, information has become available on the natural occurrence of OA in foods and feeds, its toxicity, the molds producing OA, and its role in a disease of swine and poultry in Scandinavia. Attempts are now being made to link OA to a human kidney disease. The extraordinarily rapid progress achieved in this field is, to a large extent, attributable to the great chemical stability of OA and to its fluorescent properties. These facilitated development of suitable and sensitive analytical techniques. OA and related toxins have been the subject of previous reviews.5–13