貧血是慢性腎臟病常見的併發症之一。自1990年以來使用紅血球生成素刺激劑(erythropoiesis-stimulating agent, ESA)一直是腎性貧血治療的主流。一系列大型研究顯示ESA可能存有嚴重的併發症,例如增加心血管事件和死亡的風險。目前認為這些併發症主要是跟使用ESA而非跟提高血紅素有關。口服缺氧誘導因子脯氨酰羥化酶抑制劑(hypoxia-inducible factor prolyl-hydroxylase inhibitors)藥物治療可以刺激內生性紅血球生成素的產生及提高鐵的利用性。在近年來的臨床試驗結果顯示,這些口服藥物不僅在腎性貧血的治療上有潛力取代ESA外,並且同時也可減少靜脈注射鐵的劑量及需求。
Anemia is one of the common complications of chronic kidney disease. Use of erythropoiesis-stimulating agents (ESAs) has been a mainstay of treatment for anemia since 1990. A series of large-scale clinical trials demonstrated that ESAs might induce serious complications, including cardiovascular events and mortality. It is suggested that these adverse effects might be mediated by the use of ESAs, itself, rather than the achieved target of hemoglobin level. Treatment of oral form hypoxia-inducible factor prolyl-hydroxylase inhibitors can stimulate endogenous erythropoietin production and enhance iron bioavailability. In recent clinical trials, these oral agents proved to be capable of replacing ESA therapy and minimizing the need for intravenous iron therapy for chronic kidney disease related anemia.