Abstract
The term “aristolochic acid nephropathy” (AAN) is used to include any form of toxic interstitial nephropathy that is caused either by ingestion of plants containing aristolochic acids (AA) as part of traditional phytotherapies (formerly known as “Chinese herbs nephropathy”), or by the environmental contaminants in food (Balkan endemic nephropathy). It is frequently associated with urothelial malignancies. Although products containing AA have been banned in most of countries, AAN cases remain regularly reported all over the world. Moreover, AAN incidence is probably highly underestimated given the presence of AA in traditional herbal remedies worldwide and the weak awareness of the disease. During these two past decades, animal models for AAN have been developed to investigate underlying molecular and cellular mechanisms involved in AAN pathogenesis. Indeed, a more-in-depth understanding of these processes is essential to develop therapeutic strategies aimed to reduce the global and underestimated burden of this disease. In this regard, our purpose was to build a broad overview of what is currently known about AAN. To achieve this goal, we aimed to summarize the latest data available about underlying pathophysiological mechanisms leading to AAN development with a particular emphasis on the imbalance between vasoactive factors as well as a focus on the vascular events often not considered in AAN.
Highlights
In the early 1990s, an epidemic of rapidly progressive tubulointerstitial nephritis was reported in Belgium in a cohort of young female patients
The causative nephrotoxic agent was identified as aristolochic acid (AA) [3] and this renal disease is worldwide recognized as aristolochic acid nephropathy (AAN)
AAN is certain in any individual who suffers from renal failure, in combination with at least two of the following three criteria: (i) a renal histology displaying interstitial fibrosis with a corticomedullary gradient; (ii) a history of consumption of herbal products which demonstrated the presence of AA; and (iii) the presence of AA-DNA adducts in a kidney tissue sample or of a urothelial tumor
Summary
In the early 1990s, an epidemic of rapidly progressive tubulointerstitial nephritis was reported in Belgium in a cohort of young female patients. The onset of this the renal disease was rapidly associated with the intake of slimming pills containing Chinese herbs [1,2]. Despite warnings from the Food and Drug Administration (FDA), the European Medicines Agency (EMA) and International Agency for Research on Cancer (IARC) regarding the safety of products containing AA, AAN cases remain frequently described all over the world [7,15]
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