Cruz D N, Perazella M A, Abu-Alfa A K, Mahnensmith R L
Department of Medicine, Yale University School of Medicine, New Haven, CT 06520-8029, USA.
Am J Kidney Dis. 1996 Oct;28(4):535-40. doi: 10.1016/s0272-6386(96)90464-3.
Exacerbation of anemia associated with angiotensin-converting enzyme (ACE) inhibitor therapy has been noted to occur in patients with chronic renal failure, end-stage renal disease, and renal transplantation. Angiotensin-converting enzyme inhibitors appear to cause anemia through induction of decreased red blood cell production. There are data suggesting that ACE inhibitors may impair erythropoiesis via either suppression of angiotensin-mediated erythropoietin (EPO) production or bone marrow response to EPO. Patients on chronic hemodialysis receive recombinant human EPO (rHuEPO) for therapy of anemia and may also receive an ACE inhibitor for hypertension or congestive heart failure. We undertook a retrospective study to evaluate whether patients treated with ACE inhibitors developed a more severe anemia or required a higher dose of rHuEPO to maintain a similar hematocrit. Ninety-five of 108 chronic hemodialysis patients met study criteria (hemodialysis for 4 months and no treatment with an ACE inhibitor for at least 4 months = group 1; therapy with an ACE inhibitor for at least 4 months = group 2). Forty-eight patients (group 1, n = 24; group 2, n = 24) were available for analysis after exclusion for a variety of factors. There was no difference between the two groups in terms of baseline characteristics, number of blood transfusions or hospital days, or other laboratory parameters. There was no statistically significant difference in average hematocrit between group 1 (33.5% +/- 3.9%) and group 2 (32.6% +/- 1.6%). Similarly, no significant difference was observed for the average rHuEPO dose/treatment between group 1 (3,272 +/- 1,532 IU/treatment; 50.69 +/- 26.94 IU/kg/treatment) and group 2 (3,401 +/- 1,009 IU/treatment; 52.87 +/- 19.38 IU/kg/treatment). These results suggest that ACE inhibitors do not significantly induce more severe anemia or alter rHuEPO response in chronic hemodialysis patients.
已注意到，血管紧张素转换酶（ACE）抑制剂治疗相关的贫血加重现象发生于慢性肾衰竭、终末期肾病及肾移植患者中。血管紧张素转换酶抑制剂似乎通过诱导红细胞生成减少而导致贫血。有数据表明，ACE抑制剂可能通过抑制血管紧张素介导的促红细胞生成素（EPO）生成或骨髓对EPO的反应来损害红细胞生成。接受慢性血液透析的患者接受重组人促红细胞生成素（rHuEPO）治疗贫血，也可能因高血压或充血性心力衰竭而接受ACE抑制剂治疗。我们进行了一项回顾性研究，以评估接受ACE抑制剂治疗的患者是否会出现更严重的贫血或需要更高剂量的rHuEPO来维持相似的血细胞比容。108例慢性血液透析患者中有95例符合研究标准（血液透析4个月且至少4个月未接受ACE抑制剂治疗=第1组；接受ACE抑制剂治疗至少4个月=第2组）。排除各种因素后，有48例患者（第1组，n = 24；第2组，n = 24）可供分析。两组在基线特征、输血次数或住院天数或其他实验室参数方面无差异。第1组（33.5%±3.9%）和第2组（32.6%±1.6%）的平均血细胞比容无统计学显著差异。同样，第1组（3272±1532 IU/次治疗；50.69±26.94 IU/kg/次治疗）和第2组（3401±1009 IU/次治疗；52.87±19.38 IU/kg/次治疗）的平均rHuEPO剂量/治疗也无显著差异。这些结果表明，ACE抑制剂不会在慢性血液透析患者中显著诱发更严重的贫血或改变rHuEPO反应。
