Hypovolemic Hyponatremia.

2区 医学 Q2 Medicine Frontiers of Hormone Research Pub Date : 2019-01-01 Epub Date: 2019-01-15 DOI:10.1159/000493240
Dinushika Mohottige, Ruediger Wilhelm Lehrich, Arthur Greenberg
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引用次数: 7

Abstract

The etiology of hyponatremia is often multifactorial. The most common causes include hypovolemia from gastrointestinal (GI) or other fluid losses, thiazide diuretics, and SIAD [1]. In this chapter, we will discuss hypovolemic hyponatremia, as well as the clinical parameters that help distinguish between hypovolemic and euvolemic states. These include not only the urine [Na+] concentration but also the fractional uric acid excretion, a parameter that can be employed even when diuretics have been prescribed [2,3,4,5,6,7]. Among the common causes of hypovolemic hyponatremia are GI fluid loss, a range of endocrinopathies [7], and thiazide-induced hyponatremia, which is best considered as a distinct entity, in particular because recent data suggest that it has a genetic predisposition. Also, the discontinuation of thiazide is a key step in treatment [2,7]. The management of hypovolemic hyponatremia starts with confirming its presence and determining the underlying cause. Correction focuses on the appropriate use of isotonic fluid to effect volume repletion while avoiding an overly rapid rise in serum [Na+] concentration.

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低血容量性低钠血症。
低钠血症的病因通常是多因素的。最常见的原因包括胃肠道(GI)或其他液体流失引起的低血容量、噻嗪类利尿剂和SIAD[1]。在本章中,我们将讨论低血容量性低钠血症,以及有助于区分低血容量和低血容量状态的临床参数。这些不仅包括尿[Na+]浓度,还包括分数尿酸排泄,即使在开了利尿剂后也可以使用这个参数[2,3,4,5,6,7]。低血容量性低钠血症的常见原因包括胃肠道液体流失、一系列内分泌疾病[7]和噻嗪类药物引起的低钠血症,这最好被视为一个独立的实体,特别是因为最近的数据表明它具有遗传易感性。同时,停药噻嗪是治疗的关键步骤[2,7]。低血容量性低钠血症的管理始于确认其存在并确定潜在原因。纠正的重点是适当使用等渗液来实现容量补充,同时避免血清[Na+]浓度过快上升。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Frontiers of Hormone Research
Frontiers of Hormone Research 医学-内分泌学与代谢
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期刊介绍: A series of integrated overviews on cutting-edge topics New sophisticated technologies and methodological approaches in diagnostics and therapeutics have led to significant improvements in identifying and characterizing an increasing number of medical conditions, which is particularly true for all aspects of endocrine and metabolic dysfunctions. Novel insights in endocrine physiology and pathophysiology allow for new perspectives in clinical management and thus lead to the development of molecular, personalized treatments. In view of this, the active interplay between basic scientists and clinicians has become fundamental, both to provide patients with the most appropriate care and to advance future research.
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