臺灣有25.7%的洗腎患者有糖尿病，而第二型糖尿病患有大於39.8%的比例具有微白蛋白尿（microalbuminuria）的情形；但同時有93.3%的第二型糖尿病患，正在使用口服降血糖
藥物（oral antidiabetic drugs, OADs），所以因腎功能不全引發相關藥物代謝障礙的問題，就格外引人重視。臺灣口服降血糖藥物acarbose的處方頻率由1997年的0.02%上升至2003年的4.1%（P ＜0.0001），亦為其間開方頻率竄升最快的OADs。但有關腎功能不全患者使用
acarbose的用藥安全卻常被遺忘。 以尿液中原型藥物出現的角度去評估acarbose在健康人體
之吸收率只有1.7%，但加上進入人體的代謝產物部分，則有將近35%的藥物量被吸收進入人
體，並且清除的場所皆發生在腎臟。在腎功能受損 （creatinine clearance < 25 ml/min ）的狀況下使用acarbose，其產生的藥物波鋒血中濃度及平均藥物穩態曲線下面積 （AUC：area under the curve）將會分別高於正常值的5倍及6倍。雖然目前並沒有acarbose直接造成腎毒性的相關文獻或報導，但acarbose及其代謝產物是可能在腎功能不全的狀況下於人體內蓄積，並增加不良的醫療風險。 在腎功能正常的人體試驗中亦指出服用acarbose的受試者中，有3.8 ~15%會發生有意義的肝臟酵素上升。但acarbose引起肝毒性的潛伏期，卻可於服藥後長達數星期或數月後才發生，並且未出現過敏反應表徵，故acarbose引發的肝毒性，可能起源於病患本身的代謝特異性（metabolic idiosyncrasy）。 雖然目前並無腎功能不全病患服用acarbose引發肝毒性之臨床試驗資料或病例報告，但可合理懷疑腎功能不全引發的藥物蓄積，在特定狀況下是可增加嚴重肝功能異常的不良醫療風險。因此，合併有嚴重腎衰竭的糖尿病患(creatinine clearance < 25 ml/min)，被列為acarbose之禁用族群。針對於必需使用acarbose之此類特殊族群，應考慮採取降低藥品劑量及定期肝功能監之必要措施。

In Taiwan, 25.7% of dialysis patients have diabetes mellitus and more than 39.8% of patients with type-2 diabetes have microalbuminuria. Despite of this fact, 93.3% of type-2 diabetes patients are treated with oral antidiabetic drugs (OADs), leading to great interest in relative drug metabolic disturbance caused by nephropathy.
The prescribing rate in Taiwan for acarbose rose from 0.02% in 1997 to 4.1% in 2003 (P＜0.0001). However, the safety of using acarbose has frequently been ignored in diabetic patients with nephropathy. In healthy volunteers with normal renal function, only 1.7% of an oral dose of acarbose was absorbed as an original compound.
However, approximately 35% of the ingested dosage marked with 14C was recovered in urine, indicating that its metabolites have been absorbed. In populations with renal impairment (creatinine clearance < 25 ml/min), the values of the peak plasma concentration and the mean steady-state area under the curve (AUC) of acarbose increased by five and six times normal values, respectively. Although there currently does not exist evidence that acarbose is toxic to the kidney, acarbose and its metabolites very likely accumulate in the patients with renal
impairment, causing ill-defined iatrogenic risks. In related clinical trials, significant increases in transaminases were found in 3.8~15% of patients treated with acarbose. However, the latent period of acarbose induced hepatoxicity may last up to weeks or months after ingestion and without any allergic reactions. Therefore, the mechanism of acarbose induced hepatoxicity, caused by the original compound or its metabolites, may be due to metabolic idiosyncrasy. Although there are no available clinical trial data or case reports of hepatotoxicity in the patients with renal impairment, it is reasonable to be aware of accumulation of the drug and its metabolites in particular, in such patients, as well as those with high incidence of liver abnormalities. The use of acarbose is therefore contraindicated in patients with severe renal failure. Lower dosage and enzyme monitoring are recommended for those who must be treated with acarbose.