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Hyponatremia and thiazides

机译:低钠血症和噻嗪类

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摘要

Thiazide diuretics were first introduced in 1957 and soon became recognized as a cause of hyponatremia. Thiazides are very commonly used for the treatment of hypertension and are recommended by the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC 7) as first-line therapy for uncomplicated hypertension. Thiazides can be the sole cause of hyponatremia, and they may also exacerbate hyponatremia in patients with syndrome of inappropriate antidiuretic hormone hypersecretion. Although thiazides do not inhibit the ability to concentrate urine like loop diuretics, they do impair the diluting ability by (1) inhibition of Na and Cl transport at the cortical diluting sites, (2) stimulation of vasopressin release, (3) reduction of glomerular filtration rate, and (4) enhanced proximal water reabsorption, which reduces delivery to distal diluting sites. Water retention from impaired water excretion combined with cation depletion may result in severe hyponatremia. It is recommended that thiazides be avoided in elderly frail patients with chronically high water intake, in patients who have psychogenic polydipsia, and heavy beer drinkers, as these patients depend on excretion of maximally dilute urine to maintain fluid balance.
机译:噻嗪类利尿剂于1957年首次引入,并很快被公认为是低钠血症的病因。噻嗪类非常常用于高血压的治疗,并被全国预防,检测,评估和治疗高血压联合委员会第七次报告(JNC 7)推荐为难治性高血压的一线治疗药物。噻嗪类可能是低钠血症的唯一原因,也可能加剧抗利尿激素分泌过多的综合征患者的低钠血症。尽管噻嗪类药物不像loop利尿剂那样抑制尿液的浓缩能力,但它们确实会通过(1)抑制皮质稀释部位的Na和Cl转运,(2)刺激血管加压素释放,(3)肾小球减少而削弱稀释能力(4)增强了近端水的重吸收,从而减少了向远端稀释部位的输送。排泄障碍与阳离子耗竭结合导致的水分滞留可能导致严重的低钠血症。建议在长期虚弱的慢性,高摄入水量的老年患者,精神病性多视症患者和重度饮酒者中避免使用噻嗪类药物,因为这些患者依赖于最大量稀尿的排泄来维持体液平衡。

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