Bantle J P, Nath K A, Sutherland D E, Najarian J S, Ferris T F
Arch Intern Med. 1985 Mar;145(3):505-8.
To evaluate the mechanism of cyclosporine-induced hyperkalemia, the renin-angiotensin-aldosterone system and renal potassium clearance were compared in ten renal transplant recipients treated with cyclosporine and treated with azathioprine. After stimulation by a low-sodium diet and furosemide, cyclosporine-treated patients demonstrated lower plasma renin activity when supine (1.9 +/- 0.3 v 7.8 +/- 1.4 ng/mL/hr) and after standing (3.0 +/- 0.7 v 12.2 +/- 1.5 ng/mL/hr). Supine plasma aldosterone levels tended to be lower in cyclosporine-treated patients, (4.8 +/- v 10.5 +/- 2.6 ng/dL), although standing plasma aldosterone levels were not different (10.8 +/- 3.0 v 12.3 +/- 2.0 ng/dL). After administration of 0.75 mEq of potassium chloride per kilogram of body weight, cyclosporine-treated patients excreted 52% +/- 7.1% of the potassium load in six hours compared with excretion of 67% +/- 7.0% by the azathioprine-treated patients, although there was no difference in plasma aldosterone levels in response to the potassium load in the two groups. These data suggest that cyclosporine causes suppression of plasma renin activity and a tubular insensitivity to aldosterone, both of which may impair potassium excretion.
为评估环孢素诱导高钾血症的机制,对10例接受环孢素治疗和硫唑嘌呤治疗的肾移植受者的肾素-血管紧张素-醛固酮系统及肾脏排钾情况进行了比较。在低钠饮食和速尿刺激后,接受环孢素治疗的患者仰卧时血浆肾素活性较低(1.9±0.3对7.8±1.4 ng/mL/小时),站立后也较低(3.0±0.7对12.2±1.5 ng/mL/小时)。接受环孢素治疗的患者仰卧位血浆醛固酮水平往往较低(4.8±对10.5±2.6 ng/dL),尽管站立位血浆醛固酮水平无差异(10.8±3.0对12.3±2.0 ng/dL)。给予每千克体重0.75 mEq氯化钾后,接受环孢素治疗的患者在6小时内排出了52%±7.1%的钾负荷,而接受硫唑嘌呤治疗的患者排出了67%±7.0%,尽管两组对钾负荷反应的血浆醛固酮水平无差异。这些数据表明,环孢素会抑制血浆肾素活性,并使肾小管对醛固酮不敏感,这两者都可能损害钾的排泄。