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钾离子稳态和肾素-血管紧张素-醛固酮系统抑制剂。

Potassium homeostasis and renin-angiotensin-aldosterone system inhibitors.

机构信息

Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, 22 South Greene Street, Room N3W143, Baltimore, MD 21201, USA.

出版信息

Clin J Am Soc Nephrol. 2010 Mar;5(3):531-48. doi: 10.2215/CJN.07821109. Epub 2010 Feb 11.

Abstract

Inhibition of the renin-angiotensin-aldosterone system (RAAS) is a key strategy in treating hypertension and cardiovascular and renal diseases. However, RAAS inhibitors (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, and direct renin inhibitors) increase the risk of hyperkalemia (serum potassium >5.5 mmol/L). This review evaluates the effects on serum potassium levels of RAAS inhibitors. Using PubMed, we searched for clinical trials published up to December 2008 assessing the effects on serum potassium levels of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone receptor antagonists, and direct renin inhibitors, alone and in combination, in patients with hypertension, heart failure (HF), or chronic kidney disease (CKD); 39 studies were identified. In patients with hypertension without risk factors for hyperkalemia, the incidence of hyperkalemia with RAAS inhibitor monotherapy is low (< or =2%), whereas rates are higher with dual RAAS inhibition ( approximately 5%). The incidence of hyperkalemia is also increased in patients with HF or CKD (5% to 10%). However, increases in serum potassium levels are small ( approximately 0.1 to 0.3 mmol/L), and rates of study discontinuation due to hyperkalemia are low, even in high-risk patient groups (1% to 5%). Patients with HF or CKD are at greater risk of hyperkalemia with RAAS inhibitors than those without these conditions. However, the absolute changes in serum potassium are generally small and unlikely to be clinically significant. Moreover, these patients are likely to derive benefit from RAAS inhibition. Rather than denying them an effective treatment, electrolyte levels should be closely monitored in these patients.

摘要

肾素-血管紧张素-醛固酮系统(RAAS)的抑制是治疗高血压以及心血管和肾脏疾病的主要策略。然而,RAAS 抑制剂(血管紧张素转换酶抑制剂、血管紧张素受体阻滞剂、醛固酮受体拮抗剂和直接肾素抑制剂)会增加高钾血症(血清钾 >5.5mmol/L)的风险。这篇综述评估了 RAAS 抑制剂对血清钾水平的影响。我们利用 PubMed 检索了截至 2008 年 12 月发表的评估血管紧张素转换酶抑制剂、血管紧张素受体阻滞剂、醛固酮受体拮抗剂和直接肾素抑制剂单药或联合应用对高血压、心力衰竭(HF)或慢性肾病(CKD)患者血清钾水平影响的临床试验,共检索到 39 项研究。在无高钾血症危险因素的高血压患者中,RAAS 抑制剂单药治疗时高钾血症的发生率较低(<或=2%),而双重 RAAS 抑制时发生率较高(约 5%)。HF 或 CKD 患者的高钾血症发生率也会升高(5%至 10%)。然而,血清钾水平的升高幅度较小(约 0.1 至 0.3mmol/L),且即使在高危患者群体(1%至 5%)中,因高钾血症而停止研究的比例也较低。与无这些疾病的患者相比,HF 或 CKD 患者使用 RAAS 抑制剂时发生高钾血症的风险更大。然而,血清钾的绝对变化通常较小,不太可能具有临床意义。此外,这些患者可能会从 RAAS 抑制中获益。因此,不应因担心高钾血症而拒绝为这些患者提供有效的治疗,而应密切监测其电解质水平。

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