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血管加压素过多与低钠血症。

Vasopressin excess and hyponatremia.

作者信息

Pham Phuong-Chi T, Pham Phuong-Mai T, Pham Phuong-Thu T

机构信息

Nephrology Division, Olive View-UCLA Medical Center, Sylmar, CA 91342, USA.

出版信息

Am J Kidney Dis. 2006 May;47(5):727-37. doi: 10.1053/j.ajkd.2006.01.020.

DOI:10.1053/j.ajkd.2006.01.020
PMID:16632011
Abstract

Hyponatremia is a common electrolyte disorder that frequently is overlooked and undertreated. Although the pathophysiological process of hyponatremia is complex, arginine vasopressin (AVP) is a common etiologic factor. Excess AVP release by osmotic or nonosmotic stimuli or both can lead to sodium and water imbalance. Conventional treatment options for hyponatremia, including water restriction and administration of sodium chloride with or without loop diuretics, do not directly address the underlying water retention induced by excess AVP in many cases. Clinical trials showed that AVP-receptor antagonists, including lixivaptan, tolvaptan, and conivaptan, produce aquaresis, the electrolyte-sparing excretion of free water, to correct serum sodium concentration. We review results from recent clinical trials involving AVP-receptor antagonists in the treatment of hyponatremia associated with AVP excess.

摘要

低钠血症是一种常见的电解质紊乱,常被忽视且治疗不足。尽管低钠血症的病理生理过程复杂,但精氨酸加压素(AVP)是常见的病因。渗透压或非渗透压刺激或两者共同导致的AVP过度释放可引起钠和水平衡失调。低钠血症的传统治疗方法,包括限水以及使用或不使用襻利尿剂的氯化钠给药,在许多情况下并不能直接解决AVP过多引起的潜在水潴留问题。临床试验表明,AVP受体拮抗剂,包括利伐普坦、托伐普坦和考尼伐坦,可产生利水作用,即游离水的电解质保留性排泄,以纠正血清钠浓度。我们回顾了近期涉及AVP受体拮抗剂治疗与AVP过多相关的低钠血症的临床试验结果。

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