Hyponatremia: epidemiology, pathophysiology, and therapy.
Hyponatremia: epidemiology, pathophysiology, and therapy.
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低钠血症：流行病学、病理生理学和治疗。
DOI：
10.1097/00041552-199307000-00015
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发表时间：
1993
影响因子：
3.2
通讯作者：
Verbalis,JG
中科院分区：
文献类型：
--
作者：
Verbalis,JG
尽管几十年来的研究兴趣和生产力，低钠血症和低渗透性疾病的许多方面仍然不完全了解。这些方面包括与低钠血症的发病率和死亡率有关的问题，可能的激素和性别相关的危险因素，潜在的低钠血症性脑病神经系统并发症的易感性，一些非典型亚群患者抗利尿激素分泌不当和其他低钠血症疾病对精氨酸抗利尿激素分泌的刺激。尿钠和利钠肽对低钠血症状态的贡献，低钠血症快速纠正后脑脱髓鞘的病理决定因素，以及急性和慢性低钠血症患者的适当治疗指南。最近的文献证实，这些问题和其他问题仍然没有可接受的答案，需要对低钠血症的病理生理学的基本问题有更好的了解。最近的一些进展很可能会增强我们对低钠血症和低渗透压状态的理解。首先是研究肾脏和脑组织中响应渗透压变化的体积调节的细胞机制。通过在细胞和体液室容积调节知识提供的概念框架中考虑临床观察，可以更好地理解许多临床观察，尽管显然不是全部。其次是通过互补DNA克隆阐明了几种重要的蛋白质结构，包括精氨酸抗利尿素V^和V2受体、几种有机渗透转运蛋白和CHIP28水通道。未来将这些新工具应用于精心设计和执行的生理学研究，可能会为我们对低钠血症的理解增加相当多的新知识。第三是核磁共振波谱和成像方法的发展和应用的增加，这将允许更详细地分析低钠血症期间和纠正后脑代谢的急性变化。最后，精氨酸抗利尿素V^和V2受体的非肽拮抗剂的最新发展应该使临床研究能够更准确地评估精氨酸抗利尿素对低钠血症的贡献，更重要的是为低钠血症患者提供更有效的治疗方法。
Despite several decades of research interest and productivity, many aspects of hyponatremia and hypo-osmolar disorders remain incompletely understood. Among these aspects are questions relating to the morbidity and mortality actually attributable to hyponatremia, possible hormonal and gender-associated risk factors underlying susceptibility to neurologic complications from hyponatremic encephalopathy, the stimuli to arginine vasopressin secretion in some atypical subsets of patients with the syndrome of inappropriate antidiuretic hormone secretion and other hyponatremic disorders, the contributions of natriuresis and natriuretic peptides to hyponatremic states, the pathologic determinants of brain demyelination that sometimes follow rapid correction of hyponatremia, and appropriate treatment guidelines for patients with acute and chronic hyponatremia. The recent literature confirms that acceptable answers to these questions and others are still not available, and a better understanding of basic issues regarding the pathophysiology of hyponatremia is needed. Several recent advances stand out as being likely to enhance our future understanding of hyponatremia and hypo-osmolar states. First are studies of cellular mechanisms of volume regulation in kidney and brain tissue in response to changes in osmolality. Many, though clearly not all, clinical observations can be better understood by considering them in the conceptual framework provided by knowledge of cell and body fluid compartment volume regulation. Second is the elucidation of several important protein structures via complementary DNA cloning, including the arginine vasopressin V^ and V2 receptors, several organic osmolyte transporters, and the CHIP28 water channel. Future application of these new tools to carefully designed and executed physiologic studies will likely add considerable new knowledge to our understanding of hyponatremia. Third is the development and increasing application of nuclear magnetic resonance spectroscopy and imaging methods that will allow more detailed analyses of acute changes in brain metabolism during hyponatremia and following correction. Finally, the recent development of nonpeptide antagonists to arginine vasopressin V^ and V2 receptors should enable clinical studies to assess more accurately the contribution of arginine vasopressin-induced antidiuresis to hyponatremia and more importantly holds the promise of more effective therapies for hyponatremic patients.