Vasco Raquel F V, Reis Eduardo T, Moyses Rosa M A, Elias Rosilene M
Department of Medicine, Renal Division, Hospital das Clinicas, Universidade de São Paulo, São Paulo, Brazil.
Hospital das Clinicas, Pharmacy Division, Universidade de São Paulo, São Paulo, Brazil.
Arch Osteoporos. 2017 Dec;12(1):31. doi: 10.1007/s11657-017-0326-3. Epub 2017 Mar 25.
We evaluated the effect of hydrochlorothiazide in a sample of anuric patients on hemodialysis and found an increase in serum calcium, which occurred only in those with parathyroid hormone >300 pg/ml. This finding highlights the extra-renal effect of this diuretic and a possible role of parathyroid hormone in the mechanism.
Thiazide diuretics are commonly used in patients with chronic kidney disease to treat hypertension. Their effects on calcium and bone metabolism are not well established, once calciuria may not fully explain levels of calcium and parathyroid hormone (PTH) in this population. A previous study has suggested that thiazides require the presence of PTH as a permissive condition for its renal action. In anuric patients, however, the role of PTH, if any, in the thiazide effect is unknown.
To assess thiazide extra renal effect on serum calcium and whether such an effect is reliant on PTH, hydrochlorothiazide (HCTZ) 100 mg was given orally once a day to a sample of 19 anuric patients on hemodialysis for 2 weeks. Laboratories' analyses were obtained in three phases: baseline, after diuretic use, and after a 2-week washout phase.
We demonstrated that serum calcium (Ca) increased in ten patients (52.6%) after HCTZ use, returning to previous levels after the washout period. Out of the 19 patients, ten presented PTH ≥ 300 pg/ml, and Ca has increased in eight of them, whereas in the other nine patients with PTH < 300 pg/ml, serum Ca has increased only in two individuals (RR risk of increase Ca 3.9; p = 0.012).
HCTZ was capable of increasing serum Ca in a sample of anuric patients on hemodialysis and seems this effect is highly dependent on PTH levels. Caution is required while interpreting this result, as the small sample size might implicate in a finding caused by chance.
我们评估了氢氯噻嗪对一组接受血液透析的无尿患者的影响，发现血清钙升高，且仅在甲状旁腺激素>300 pg/ml的患者中出现。这一发现突出了这种利尿剂的肾外作用以及甲状旁腺激素在该机制中可能发挥的作用。
噻嗪类利尿剂常用于慢性肾脏病患者以治疗高血压。它们对钙和骨代谢的影响尚未完全明确，因为尿钙可能无法完全解释该人群中的钙和甲状旁腺激素（PTH）水平。先前的一项研究表明，噻嗪类药物发挥肾脏作用需要有PTH作为允许条件。然而，在无尿患者中，PTH在噻嗪类药物作用中的作用（如果有）尚不清楚。
为了评估噻嗪类药物对血清钙的肾外作用以及这种作用是否依赖于PTH，对19例接受血液透析的无尿患者样本口服100 mg氢氯噻嗪（HCTZ），每日1次，持续2周。分三个阶段进行实验室分析：基线期、使用利尿剂后以及2周的洗脱期后。
我们证明，使用HCTZ后，10例患者（52.6%）的血清钙（Ca）升高，洗脱期后恢复到先前水平。在19例患者中，10例患者的PTH≥300 pg/ml，其中8例患者的钙升高，而在其他9例PTH<300 pg/ml的患者中，仅2例患者的血清钙升高（钙升高的相对风险为3.9；p = 0.012）。
HCTZ能够使接受血液透析的无尿患者样本中的血清钙升高，且这种作用似乎高度依赖于PTH水平。解释这一结果时需谨慎，因为样本量较小可能导致结果是偶然发现。
