Recently, an article published in the authoritative journal Science Translational Medicine stated that “toxic herbs containing aristolochic acid and related compounds may be an important cause of liver cancer in Asia, especially in mainland China and Taiwan.” With the release of the article, the under-appreciated name “aristolochic acid” was hotly debated by all medical media, and its toxic effects once again became the focus of attention – after all, whether it’s liver damage, cancer, kidney damage, or urinary tract damage, it’s no It is not a joke. Today, I have organized the nephrotoxicity of aristolochic acid, its mechanism and common drugs for your reference. What is aristolochic acid? Aristolochic acid (AA) is a class of nitrophilic compounds found in plants of the Aristolochiaceae family, and is a general term for a group of chemical components. Common herbal and proprietary Chinese medicines containing aristolochic acid include: What is aristolochic acid nephropathy? Aristolochic acid nephropathy (AAN) refers to interstitial renal tubular disease caused by the use of herbal medicines containing aristolochic acid. The pathogenesis is not well understood, but may involve the following aspects: Direct toxic injury AA and its metabolites have a direct damaging effect on the kidney, and the target cells are mainly the proximal tubular epithelial cells. It can lead to necrosis, apoptosis, transdifferentiation, or decreased protein reabsorption of epithelial cells. Inhibition of cell repair AA and its metabolites inhibit cell proliferation and repair while directly damaging cells, and the mechanism of AA inhibition of cell proliferation and repair may be related to cell cycle arrest and decreased growth factor expression. Induced transdifferentiation of renal tubular epithelial cells to fibroblasts The persistence of low-dose AA or long-term repeated stimulation can induce transdifferentiation of renal tubular epithelial cells to mesenchymal cells and the development of residual tubular interstitial fibrosis, which in turn causes progressive kidney injury. Local ischemia and hypoxia in the kidney AA can directly damage renal vascular endothelial cells, resulting in a reduction of renal interstitial microvasculature, and can also damage renal tubular epithelial cells, resulting in an imbalance of vasoactive substances, thus causing local ischemia and hypoxia in the renal interstitium Clinical manifestations of aristolochic acid nephropathy Aristolochic acid nephropathy mostly develops after middle age, and is more common in women, with three types of onset: Acute AAN is only seen in a very small number of patients, often due to a short period of time It is often caused by continuous or overdose of aqueous decoction of Chinese medicine containing AA. Clinical manifestations are oliguric or non-oliguric acute renal failure, which may be accompanied by nausea, vomiting, anemia, thrombocytopenia, and liver function impairment. There is usually no hypertension and the urinalysis is mild. Renal tubular dysfunction Patients often develop weakness, thirst, excessive drinking, polyuria and nocturia several weeks to months after taking small doses of aristolochic acid-containing Chinese medicine, mainly manifesting as renal tubular acidosis and/or Fanconi syndrome, accompanied by renal tubular concentration dysfunction, while blood creatinine and urea nitrogen are basically normal. Chronic AAN accounts for the majority of the disease. Patients often have a history of long-term or intermittent repeated use of AA-containing proprietary Chinese medicines, with insidious clinical manifestations, and may have discontinued their medication for several years at the time of onset, with features consistent with the general characteristics of chronic interstitial nephritis, mostly manifesting as progressive renal failure, often accompanied by anemia and hypertension. The diagnosis of aristolochic acid nephropathy has no internationally or nationally accepted diagnostic criteria. The clinical diagnosis of this disease is based on a clear history of drug use, clinical manifestations of markedly impaired tubular function and/or decreased glomerular function, and typical pathological manifestations. Prevention and prognosis of aristolochic acid nephropathy AAN has become a common cause of acute and chronic renal insufficiency in clinical practice, and there is a lack of effective prevention and treatment methods, and patients have a poor prognosis, with most patients having irreversible lesions and renal function. the key to prevention and treatment of AAN is to strengthen the standard management of herbal medicine and prevent its onset. It is worth noting that not all people taking herbal medicines containing AAs will develop AAN. Elucidating the individual susceptibility to AAN and the pathophysiological mechanism of its progressive development is of great practical significance not only for the correct understanding of AAN, but also for the rational use of herbal medicines and the prevention of herbal medicine related kidney damage.