Conlon P J, Kovalik E, Schumm D, Minda S, Schwab S J
Department of Medicine, Duke University, Medical Center, Durham, NC 27710, USA.
Ren Fail. 2000;22(4):435-44. doi: 10.1081/jdi-100100885.
Since the earliest reports of the use of Epoetin alfa in hemodialysis patients, it has been described that Epoetin alfa may exacerbate preexisting hypertension or induce hypertension in End Stage Renal Disease (ESRD) patients not previously hypertensive. We undertook this study to determine if the correction of anemia in ESRD patients with cardiac disease from a hematocrit of 30+/-3% to 42+/-3% with the use of Epoetin alfa would result in increased blood pressure. This study was a substudy of the "Normal hematocrit Study".
Thirty-one patients were randomized into one of two arms. Patients in Group A had their hematocrit increased with the use of slowly escalating doses of Epoetin alfa to 42+/-3% and patients in Group B were maintained with a hematocrit of 30+/-3% throughout the course of the study. All patients had their blood pressure recorded with a 24 hour ambulatory BP device at study entry and at 28 weeks following randomization when they had achieved their target hematocrit. Pre-dialysis systolic and diastolic BP was also recorded.
The mean hematocrit increased in Group A from 29.1+/-2.4% to 40.8+/-5.2% after 30 weeks. The hematocrit in Group B remained stable at 30+/-3% throughout the course of the study. There was no difference in mean daytime, mean nighttime or 24 hour systolic or diastolic blood pressure between Groups A and B at either baseline or follow-up. Neither was there a difference in mean pre-dialysis systolic or diastolic BP between Groups A or B at baseline or Follow-up. Four patients in Group A and 4 patients in Group B required an increase in their antihypertensive medication during the course of the study.
It is possible to increase hematocrit to normal levels in hemodialysis with the administration of Epoetin alfa. The increase in hematocrit from 30+/-3% to 42+/-3% is not associated with increased blood pressure.
自最早报道在血液透析患者中使用促红细胞生成素α以来，已有描述称促红细胞生成素α可能会使已有的高血压加重，或在既往无高血压的终末期肾病（ESRD）患者中诱发高血压。我们开展这项研究以确定，使用促红细胞生成素α将患有心脏病的ESRD患者的血细胞比容从30±3%纠正至42±3%是否会导致血压升高。本研究是“正常血细胞比容研究”的一项子研究。
31名患者被随机分为两组。A组患者通过使用剂量逐渐增加的促红细胞生成素α将血细胞比容提高至42±3%，B组患者在整个研究过程中血细胞比容维持在30±3%。所有患者在研究入组时以及随机分组后28周达到目标血细胞比容时，均使用24小时动态血压监测仪记录血压。还记录了透析前的收缩压和舒张压。
30周后，A组的平均血细胞比容从29.1±2.4%升至40.8±5.2%。B组的血细胞比容在整个研究过程中保持稳定，为30±3%。A组和B组在基线或随访时的日间平均、夜间平均或24小时收缩压或舒张压均无差异。A组和B组在基线或随访时的透析前平均收缩压或舒张压也无差异。在研究过程中，A组有4名患者和B组有4名患者需要增加抗高血压药物剂量。
通过给予促红细胞生成素α可使血液透析患者的血细胞比容升至正常水平。血细胞比容从30±3%升至42±3%与血压升高无关。
