COMPARISON OF ENALAPRIL AND LOSARTAN IN POST TRANSPLANT ERYTHROCYTOSIS

依那普利和氯沙坦治疗移植后红细胞增多症的比较

• 批准号: 5215692
• 负责人: BRUCE A JULIAN
• 金额: --
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/5215692
• 关键词: antihypertensive agents; clinical research; drug screening /evaluation; enalapril; erythrocytes; human subject; human therapy evaluation; kidney transplantation

Angiotensin-converting enzyme inhibitors reliably reduce hematocrits in renal transplant patients with erythrocytosis, through an undefined mechanism, independent of changes in circulating erythropoietin. We treated 18 patients with posttransplant erythrocytosis with losartan, which antagonizes action of angiotensin II by binding to its receptor. Eleven patients whose hematocrits increased by at least 4 percentage points after withdrawal of enalapril (from 45.4 +/- 52.0 +/- 3.4 by 8-12 weeks after withdrawal), and 7 previously untreated patients with hematocrit 52.9 +/- 2.0 were studied. Dosage of losartan was 25 or 50 mg per day. We measured hematocrit, serum potassium and creatinine levels, and mean arterial blood pressure at 4-week intervals. Hematocrit decreased significantly after 8 weeks of losartan treatment. In 15 patients on therapy for 12 weeks the hematocrit has further decreased to 48.9 +/- 4.8 (p=0.007 compared to their pretreatment baseline). At last follow-up, the hematocrit has decreased by at least 4 points in 15 of 18 (83%) patients. Assays for measurement of plasma erythropoietin, angiotensin II, and peripheral renin activity have not yet been completed. Therapy was well tolerated. Although the serum potassium level increased and mean arterial blood pressure decreased significantly, no patient withdrew due to severe hyperkalemia or symptomatic hypotension. Thus, losartan effectively reduced hematocrit in patients with posttransplant erythrocytosis. This effect implies that angiotensin II stimulates erythropoiesis in some renal transplant patients, directly or indirectly.

血管紧张素转换酶抑制剂可靠地降低患者的红细胞压积 肾移植患者红细胞增多症，通过一种未定义的 机制，不依赖于循环中促红细胞生成素的变化。我们 氯沙坦治疗移植后红细胞增多症18例 它通过与血管紧张素II的受体结合来对抗血管紧张素II的作用。 11例血细胞计数升高至少4%的患者 停用依那普利后积分(8-12年前45.4+/-52.0+/-3.4 停药后几周)，以及7名以前未接受治疗的患者 红细胞压积52.9+/-2.0。氯沙坦的剂量为25或50 每天服用毫克。我们测量了红细胞压积、血钾和肌酐 以及每隔4周的平均动脉压。 氯沙坦治疗8周后，红细胞压积明显降低。 在接受治疗12周的15名患者中，红细胞压积进一步 降至48.9%+/-4.8%(P=0.007 基线)。最后一次随访时，红细胞压积至少降低了 18例患者中15例(83%)评分为4分。测定血浆的几种方法 促红细胞生成素、血管紧张素II和外周肾素活性没有 还没有完工。治疗耐受性良好。虽然血清 血钾水平升高，平均动脉压下降 值得注意的是，没有患者因严重的高钾血症或 症状性低血压。 因此，氯沙坦可有效降低慢性阻塞性肺疾病患者的红细胞压积。 移植后红细胞增多症。这一效应意味着血管紧张素II 直接或间接刺激某些肾移植患者的红细胞生成 间接的。