Gehr T W, Sica D A, Brater C, Davis J, Fakhry I
Department of Medicine, Medical College of Virginia, Richmond 23298-0001.
Clin Pharmacol Ther. 1988 May;43(5):547-53. doi: 10.1038/clpt.1988.71.
Furosemide was administered intravenously to four patients who had undergone renal transplantation in the past and four creatinine clearance--matched control subjects. Both patients who had undergone renal transplant and control subjects displayed similar pharmacokinetic and pharmacodynamic behavior, as assessed by drug delivery to the urine and sodium excretion, respectively. Despite similar degrees of natriuresis, patients who had undergone renal transplantation demonstrated a clear defect in urine potassium excretion. This defect in potassium excretion was not related to altered responsiveness of the renin-angiotensin-aldosterone axis because plasma renin activity increased in a normal fashion after furosemide in both control and transplant subjects. Although the plasma aldosterone response to increases in plasma renin activity was sluggish in patients undergoing renal transplantation, normal increases in plasma aldosterone levels were achieved in both groups, suggesting that there may be an intrinsic defect in distal tubular potassium secretion that can be unmasked by furosemide.
对4例既往接受过肾移植的患者及4例肌酐清除率匹配的对照受试者静脉注射呋塞米。分别通过尿液中的药物排泄和钠排泄评估发现，接受肾移植的患者和对照受试者表现出相似的药代动力学和药效学行为。尽管钠利尿程度相似，但接受肾移植的患者在尿钾排泄方面存在明显缺陷。这种钾排泄缺陷与肾素 - 血管紧张素 - 醛固酮轴反应性改变无关，因为在对照受试者和肾移植受试者中，呋塞米给药后血浆肾素活性均以正常方式升高。虽然接受肾移植患者的血浆醛固酮对血浆肾素活性升高的反应迟缓，但两组血浆醛固酮水平均实现了正常升高，这表明远曲小管钾分泌可能存在内在缺陷，呋塞米可揭示这一缺陷。
