Haase Volker H, Tanaka Tetsuhiro, Koury Mark J
Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center and Vanderbilt University School of Medicine, Nashville, TN.
Medical and Research Service, Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN.
Hematology Am Soc Hematol Educ Program. 2024 Dec 6;2024(1):409-418. doi: 10.1182/hematology.2024000655.
Anemia is a hallmark of chronic kidney disease (CKD), worsens with disease progression, and profoundly affects a patient's well-being. Major pathogenic factors are inadequate kidney erythropoietin (EPO) production and absolute and functional iron deficiency. The 2 mainstays of current anemia treatment are a) replacement therapy with recombinant EPO or 1 of its glycosylated derivatives, administered subcutaneously or intravenously, and b) intravenous (IV) iron injections. Over the past 5 years, hypoxia-inducible factor (HIF)-prolyl hydroxylase inhibitors (HIF-PHIs) have been approved in many countries for the management of anemia in both nondialysis and dialysis-dependent patients with CKD. Due to cardiovascular safety concerns, only 2 HIF-PHIs, daprodustat and vadadustat, have been approved for marketing in the United States, and only for patients on maintenance dialysis. HIF-PHIs are oral agents that are effective at improving and maintaining hemoglobin levels by activating HIF signaling in anemic patients with CKD. They stimulate the production of endogenous EPO, increase total iron-binding capacity through their direct effects on transferrin gene transcription, lower plasma hepcidin indirectly, and have beneficial effects on red blood cell parameters. Here, we discuss the mechanisms of action and pharmacologic properties of different HIF-PHIs. We discuss unwanted on-target and off-target effects, review cardiovascular and other safety concerns, and provide a benefit/risk-based perspective on how this new class of oral drugs might impact current anemia management in CKD. A clinical case is presented that highlights the clinical complexities and therapeutic challenges in managing anemia in CKD.
贫血是慢性肾脏病(CKD)的一个特征,会随着疾病进展而恶化,并严重影响患者的健康。主要致病因素是肾脏促红细胞生成素(EPO)产生不足以及绝对铁缺乏和功能性铁缺乏。当前贫血治疗的两大主要方法是:a)用重组EPO或其糖基化衍生物之一进行替代治疗,通过皮下或静脉注射给药;b)静脉注射铁剂。在过去5年中,缺氧诱导因子(HIF)-脯氨酰羟化酶抑制剂(HIF-PHIs)已在许多国家被批准用于治疗非透析和依赖透析的CKD患者的贫血。由于心血管安全性问题,在美国只有两种HIF-PHIs(达普司他和伐达司他)被批准上市,且仅适用于维持性透析患者。HIF-PHIs是口服药物,通过激活CKD贫血患者的HIF信号通路,有效改善和维持血红蛋白水平。它们刺激内源性EPO的产生,通过对转铁蛋白基因转录的直接作用增加总铁结合能力,间接降低血浆铁调素水平,并对红细胞参数产生有益影响。在此,我们讨论不同HIF-PHIs的作用机制和药理特性。我们讨论不良的靶向和非靶向效应,回顾心血管和其他安全性问题,并基于获益/风险的角度探讨这类新型口服药物可能如何影响当前CKD贫血的管理。本文介绍了一个临床病例,突出了CKD贫血管理中的临床复杂性和治疗挑战。