The potassium regulator patiromer affects serum and stool electrolytes in patients receiving hemodialysis
The potassium regulator patiromer affects serum and stool electrolytes in patients receiving hemodialysis
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DOI：
10.1016/j.kint.2020.06.042
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发表时间：
2020-11-01
影响因子：
19.6
通讯作者：
Raj, Dominic S.
中科院分区：
文献类型：
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作者：
Amdur, Richard L.;Paul, Rohan;Raj, Dominic S.
高钾血症是维持性血液透析患者常见且重要的死亡原因。在这里，我们研究了合成阳离子交换剂Patiromer对钾稳态的调节作用。对27例无尿高钾血症血液透析患者(主要为2mEq/L透析液)在连续2周不治疗、治疗12周(16.8g/d)和6周(不治疗)的过程中测定了血清和粪便电解质。血钾由治疗前的平均值5.7mEq/L降至治疗中的5.1mEq/L，治疗后回升至5.4mEq/L。治疗期间血清钙显著升高(从8.9 mg/dL降至9.1 mg/dL)，血清镁显著下降(从2.6 mg/dL降至2.4 mg/dL)。血清镁每升高一次，血钾升高1.07mEq/L，大便钾值由治疗前(4132~5923mEg/g)显著升高，治疗后显著下降至4246mEq/g，大便钾每增加一亩，血钾显著下降0.05mEq/L，大便钙(13017 mEq/g)显著高于治疗前(7874mUg/g)和治疗后(7635mEg/g)。我们估计16.8g的地塞米松可使粪钾增加1880mug/g，使血钾降低0.5mEq/L。因此，在地塞米松的治疗过程中，粪便与血钾、钙、镁之间存在复杂的相互作用。帕金森引起的血清钙和镁变化的长期后果仍有待研究。
Hyperkalemia is a common and an important cause of death in maintenance hemodialysis patients. Here we investigated the effect of patiromer, a synthetic cation exchanger, to regulate potassium homeostasis. Serum and stool electrolytes were measured in 27 anuric patients with hyperkalemia receiving hemodialysis (mainly 2 mEq/L dialysate) during consecutive two weeks of no-treatment, 12 weeks of treatment with patiromer (16.8g once daily), and six weeks of no treatment. The serum potassium decreased from a mean of 5.7 mEq/L pre-treatment to 5.1 mEq/L during treatment and rebounded to 5.4 mEq/L post-treatment. During the treatment phase, serum calcium significantly increased (from 8.9 to 9.1 mg/dL) and serum magnesium significantly decreased (from 2.6 to 2.4 mg/dL) compared to pre-treatment levels. For each one mEg/L increase in serum magnesium, serum potassium increased by 1.07 mEq/L. Stool potassium significantly increased during treatment phase from pre-treatment levels (4132 to 5923 mu g/g) and significantly decreased post-treatment to 4246 mu g/g. For each one mu gig increase in stool potassium, serum potassium significantly declined by 0.05 mEq/L. Stool calcium was significantly higher during the treatment phase (13017 mu g/g) compared to pre-treatment (7874 mu g/ g) and post-treatment (7635 mu g/g) phases. We estimated that 16.8 g of patiromer will increase fecal potassium by 1880 mu g/g and reduce serum potassium by 0.5 mEq/L. Thus, there is a complex interaction between stool and blood potassium, calcium and magnesium during patiromer treatment. Long term consequence of patiromer-induced changes in serum calcium and magnesium remains to be studied.