Bakris G L, Siomos M, Richardson D, Janssen I, Bolton W K, Hebert L, Agarwal R, Catanzaro D
Hypertension/Clinical Research Center, Rush University, Chicago, Illinois 60612, USA.
Kidney Int. 2000 Nov;58(5):2084-92. doi: 10.1111/j.1523-1755.2000.00381.x.
BACKGROUND: Inhibition of the renin-angiotensin system is known to raise serum potassium [K(+)] levels in patients with renal insufficiency or diabetes. No study has evaluated the comparative effects of an angiotensin-converting enzyme (ACE) inhibitor versus an angiotensin receptor blocker (ARB) on the changes in serum [K(+)] in people with renal insufficiency. METHODS: The study was a multicenter, randomized, double crossover design, with each period lasting one month. A total of 35 people (21 males and 14 females, 19 African Americans and 16 Caucasian) participated, with the mean age being 56 +/- 2 years. Mean baseline serum [K(+)] was 4.4 +/- 0.1 mEq/L. The glomerular filtration rate (GFR) was 65 +/- 5 mL/min/1.73 m(2), and blood pressure was 150 +/- 2/88 +/- 1 mm Hg. The main outcome measure was the difference from baseline in the level of serum [K+], plasma aldosterone, and GFR following the initial and crossover periods. RESULTS: For the total group, serum [K(+)] changes were not significantly different between the lisinopril or valsartan treatments. The subgroup with GFR values of < or = 60 mL/min/1.73 m(2) who received lisinopril demonstrated significant increases in serum [K(+)] of 0.28 mEq/L above the mean baseline of 4.6 mEq/L (P = 0.04). This increase in serum [K(+)] was also accompanied by a decrease in plasma aldosterone (P = 0.003). Relative to the total group, the change in serum [K(+)] from baseline to post-treatment in the lisinopril group was higher among those with GFR values of < or = 60 mL/min/1.73 m(2). The lower GFR group taking valsartan, however, demonstrated a smaller rise in serum [K(+)], 0.12 mEq/L above baseline (P = 0.1), a 43% lower value when compared with the change in those who received lisinopril. This blunted rise in [K(+)] in people taking valsartan was not associated with a significant decrease in plasma aldosterone (P = 0.14). CONCLUSIONS: In the presence of renal insufficiency, the ARB valsartan did not raise serum [K(+)] to the same degree as the ACE inhibitor lisinopril. This differential effect on serum [K(+)] is related to a relatively smaller reduction in plasma aldosterone by the ARB and is not related to changes in GFR. This study provides evidence that increases in serum [K(+)] are less likely with ARB therapy compared with ACE inhibitor therapy in people with renal insufficiency.
背景：已知抑制肾素 - 血管紧张素系统会使肾功能不全或糖尿病患者的血清钾[K⁺]水平升高。尚无研究评估血管紧张素转换酶（ACE）抑制剂与血管紧张素受体阻滞剂（ARB）对肾功能不全患者血清[K⁺]变化的比较效果。 方法：该研究采用多中心、随机、双交叉设计，每个阶段持续一个月。共有35人（21名男性和14名女性，19名非裔美国人及16名白种人）参与，平均年龄为56±2岁。平均基线血清[K⁺]为4.4±0.1 mEq/L。肾小球滤过率（GFR）为65±5 mL/min/1.73 m²，血压为150±2/88±1 mmHg。主要观察指标为初始期和交叉期后血清[K⁺]水平、血浆醛固酮和GFR与基线的差异。 结果：对于整个研究组，赖诺普利或缬沙坦治疗后血清[K⁺]的变化无显著差异。接受赖诺普利治疗的GFR值≤60 mL/min/1.73 m²的亚组，血清[K⁺]较平均基线4.6 mEq/L显著升高0.
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