Son Raku, Nagahama Masahiko, Tanemoto Fumiaki, Ito Yugo, Taki Fumika, Tsugitomi Ryosuke, Nakayama Masaaki
Department of Nephrology, St. Luke's International Hospital, Tokyo, Japan.
Department of Pulmonary Medicine, Thoracic Center, St. Luke's International Hospital, Tokyo, Japan.
Endocrinol Diabetes Metab Case Rep. 2020 May 13;2020. doi: 10.1530/EDM-19-0155.
The etiology of hyponatremia is assessed based on urine osmolality and sodium. We herein describe a 35-year-old Asian man with pulmonary tuberculosis and perforated duodenal ulcer who presented with hyponatremia with hourly fluctuating urine osmolality ranging from 100 to 600 mosmol/kg, which resembled urine osmolality observed in typical polydipsia and SIADH simultaneously. Further review revealed correlation of body temperature and urine osmolality. Since fever is a known non-osmotic stimulus of ADH secretion, we theorized that hyponatremia in this patient was due to transient ADH secretion due to fever. In our case, empiric exogenous glucocorticoid suppressed transient non-osmotic ADH secretion and urine osmolality showed highly variable concentrations. Transient ADH secretion-related hyponatremia may be underrecognized due to occasional empiric glucocorticoid administration in patients with critical illnesses. Repeatedly monitoring of urine chemistries and interpretation of urine chemistries with careful review of non-osmotic stimuli of ADH including fever is crucial in recognition of this etiology.
Hourly fluctuations in urine osmolality can be observed in patients with fever, which is a non-osmotic stimulant of ADH secretion. Repeated monitoring of urine chemistries aids in the diagnosis of the etiology underlying hyponatremia, including fever, in patients with transient ADH secretion. Glucocorticoid administration suppresses ADH secretion and improves hyponatremia even in the absence of adrenal insufficiency; the etiology of hyponatremia should be determined carefully in these patients.
基于尿渗透压和尿钠评估低钠血症的病因。我们在此描述一名35岁的亚洲男性，患有肺结核和十二指肠溃疡穿孔，出现低钠血症，每小时尿渗透压波动范围为100至600 mosmol/kg，这类似于典型的烦渴症和抗利尿激素分泌不当综合征（SIADH）同时出现时观察到的尿渗透压。进一步检查发现体温与尿渗透压相关。由于发热是已知的抗利尿激素分泌的非渗透性刺激因素，我们推测该患者的低钠血症是由于发热引起的短暂抗利尿激素分泌所致。在我们的病例中，经验性给予外源性糖皮质激素抑制了短暂的非渗透性抗利尿激素分泌，尿渗透压显示出高度可变的浓度。由于在危重病患者中偶尔会经验性使用糖皮质激素，与短暂抗利尿激素分泌相关的低钠血症可能未得到充分认识。反复监测尿化学指标并结合仔细审查包括发热在内的抗利尿激素的非渗透性刺激因素来解释尿化学指标，对于识别这种病因至关重要。
发热患者可观察到每小时尿渗透压的波动，发热是抗利尿激素分泌的非渗透性刺激因素。反复监测尿化学指标有助于诊断低钠血症的潜在病因，包括短暂抗利尿激素分泌患者的发热。即使在没有肾上腺功能不全的情况下，给予糖皮质激素也能抑制抗利尿激素分泌并改善低钠血症；对于这些患者，应仔细确定低钠血症的病因。
