COMPARISON OF ENALAPRIL AND LOSARTAN IN POST TRANSPLANT ERYTHROCYTOSIS

血管紧张素转换酶抑制剂可靠地降低 肾移植患者红细胞增多症，通过一个不确定的 机制，独立于循环促红细胞生成素的变化。 我们 用氯沙坦治疗18例移植后红细胞增多症患者， 其通过与血管紧张素II的受体结合而拮抗血管紧张素II的作用。 11例患者的血细胞比容增加至少4% 依那普利停药后的评分（从45.4 +/- 52.0 +/- 3.4，8-12 停药后7周）和7例既往未接受过治疗的患者， 血细胞比容为52.9 +/-2.0。 氯沙坦的剂量为25或50 毫克/天。 我们测量了红细胞压积、血清钾和肌酐 水平和平均动脉血压，每隔4周。 氯沙坦治疗8周后，红细胞压积显著下降。 在15名接受12周治疗的患者中， 降低至48.9 +/- 4.8（与治疗前相比，p=0.007 基线）。 在最后一次随访时，红细胞压积至少降低了 18例患者中有15例（83%）4分。血浆测定法 促红细胞生成素、血管紧张素II和外周血肾素活性 尚未完成。 治疗耐受性良好。 虽然血清 钾水平升高，平均动脉血压降低 值得注意的是，没有患者因重度高钾血症或 症状性低血压 因此，氯沙坦有效地降低了患者的红细胞压积 移植后红细胞增多症 这种效应意味着血管紧张素II 在一些肾移植患者中，直接或 间接地。

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.