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抗利尿激素分泌失调综合征中精氨酸加压素的调节

Regulation of arginine vasopressin in the syndrome of inappropriate antidiuresis.

作者信息

Robertson Gary L

机构信息

Division of Endocrinology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.

出版信息

Am J Med. 2006 Jul;119(7 Suppl 1):S36-42. doi: 10.1016/j.amjmed.2006.05.006.

Abstract

The syndrome of inappropriate antidiuresis (SIAD) is a disorder of sodium and water balance characterized by hypotonic hyponatremia and impaired water excretion in the absence of renal insufficiency, adrenal insufficiency, or any recognized stimulus for the antidiuretic hormone arginine vasopressin (AVP). Hyponatremia is primarily a result of excessive water retention caused by a combination of excessive intake and inappropriate antidiuresis. It is sometimes aggravated by a sodium deficiency caused by decreased intake and/or a secondary natriuresis triggered by and largely corrective of the increase in extracellular volume. Hence, there is neither edema nor signs of hypovolemia. Inappropriate antidiuresis is usually due to administration or endogenous production of AVP or another vasopressin receptor agonist such as desmopressin. Endogenous production can be either ectopic (from a tumor) or eutopic (from the neurohypophysis). The latter apparently is induced by a wide variety of diseases, drugs, or injuries and is divisible into 3 different types of abnormal AVP release during hypertonic saline infusion: high, erratic fluctuations unrelated to increases in plasma sodium (type A); a slow constant "leak" that is also unaffected by increases in plasma sodium (type B); and rapid progressive increases in plasma AVP that correlate closely with plasma sodium as it rises toward the normal range (type C or "reset osmostat"). In 5% to 10% of patients, there is no demonstrable abnormality in the osmoregulation of AVP (type D) and the cause of inappropriate antidiuresis is unclear. In some children it appears to be due to an activating mutation of the V2 receptor (V2R). In other patients, it may be due to abnormal control of aquaporin-2 water channels in renal collecting tubules or production of an antidiuretic principle other than AVP. These different types of osmoregulatory dysfunction underlying SIAD may result in marked differences in clinical presentation or response to therapy with fluid restriction, hypertonic saline infusion, or vasopressin antagonists.

摘要

抗利尿激素分泌失调综合征(SIAD)是一种钠和水平衡紊乱疾病,其特征为低渗性低钠血症以及在无肾功能不全、肾上腺功能不全或任何已知抗利尿激素精氨酸加压素(AVP)刺激因素的情况下水排泄受损。低钠血症主要是由于摄入过多和抗利尿不当共同导致的水潴留过多所致。有时,因摄入量减少引起的钠缺乏和/或由细胞外液量增加引发并在很大程度上对其进行纠正的继发性利钠作用会使其加重。因此,既没有水肿也没有血容量不足的体征。抗利尿不当通常是由于AVP的给药或内源性产生,或另一种血管加压素受体激动剂如去氨加压素所致。内源性产生可能是异位性的(源于肿瘤)或原位性的(源于神经垂体)。后者显然是由多种疾病、药物或损伤诱发的,在高渗盐水输注期间可分为3种不同类型的异常AVP释放:高、与血浆钠升高无关的不稳定波动(A型);不受血浆钠升高影响的缓慢持续“渗漏”(B型);以及随着血浆钠向正常范围升高而与血浆钠密切相关的血浆AVP快速进行性增加(C型或“渗透压调定点重置”)。在5%至10%的患者中,AVP的渗透压调节没有可证实的异常(D型),抗利尿不当的原因尚不清楚。在一些儿童中,这似乎是由于V2受体(V2R)的激活突变所致。在其他患者中,可能是由于肾集合管中水通道蛋白-水通道2的异常调控或除AVP外的抗利尿物质的产生。SIAD潜在的这些不同类型的渗透压调节功能障碍可能导致临床表现或对限液、高渗盐水输注或血管加压素拮抗剂治疗的反应存在显著差异。

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