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Diagnostic algorithm of hyponatremia. 低钠血症的诊断算法。
Pub Date : 2025-10-08 DOI: 10.1016/j.beem.2025.102053
Rose Lin, Mathis Grossmann, Annabelle M Warren

Hyponatremia is the most common electrolyte disturbance and is associated with increased morbidity and mortality. It is driven by an excess of free water relative to total body sodium. While determining the underlying cause(s) of hyponatremia can be challenging, this can be facilitated by an algorithmic approach. Hypotonic hyponatremia is diagnosed by excluding translocational and pseudohyponatremia and confirmed by measuring plasma osmolality. Measuring urine osmolality and urine sodium concentration together with clinical history and examination, especially assessment of volume status, can determine the underlying cause. The most common cause of hyponatremia is the syndrome of inappropriate diuresis, characterised by inappropriate arginine vasopressin activity resulting a high urine osmolality and high urine sodium concentration. Further investigation can determine the underlying cause(s) of the syndrome of inappropriate antidiuresis. This review provides a diagnostic algorithm for hyponatremia, with a focus on biochemical parameters supplemented by clinical fluid status examination.

低钠血症是最常见的电解质紊乱,与发病率和死亡率增加有关。它是由游离水相对于全身钠的过量所驱动的。虽然确定低钠血症的潜在原因可能具有挑战性,但这可以通过算法方法来促进。低渗性低钠血症通过排除易位性和假性低钠血症来诊断,并通过测量血浆渗透压来确诊。测量尿渗透压和尿钠浓度,结合临床病史和检查,特别是评估容量状态,可以确定潜在的原因。低钠血症最常见的原因是不适当利尿综合征,其特征是不适当的精氨酸抗利尿素活性导致高尿渗透压和高尿钠浓度。进一步的调查可以确定不适当的抗利尿综合征的根本原因。本文综述了一种低钠血症的诊断算法,以生化参数为重点,辅以临床体液状态检查。
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引用次数: 0
Special considerations of hyponatremia in the elderly patient. 老年患者低钠血症的特殊考虑。
Pub Date : 2025-09-26 DOI: 10.1016/j.beem.2025.102040
Julie Refardt

Hyponatremia is the most common electrolyte disorder, particularly in older adults. Its high prevalence in this population is driven by underlying conditions such as heart and kidney failure, as well as by factors like polypharmacy and malnutrition. Rising global temperatures have also been linked to increased hyponatremia rates. Chronic hyponatremia is associated with elevated risks of falls, osteoporosis, fractures, cognitive and muscular impairment, and mortality. Despite these adverse outcomes, the condition is often underdiagnosed and undertreated, partly due to the complexity of its evaluation. Simplified, step-by-step diagnostic algorithms in future guidelines may help address this gap. Evidence increasingly supports the clinical benefits of correcting hyponatremia, prompting investigation into novel therapies. Among these, SGLT2 inhibitors and protein supplementation are especially promising, offering efficacy not only in raising plasma sodium but also in providing broader health benefits. This review explores the impact of hyponatremia in the elderly, summarizes its leading causes, and evaluates diagnostic strategies alongside the advantages and limitations of current treatment options.

低钠血症是最常见的电解质紊乱,尤其是在老年人中。其在这一人群中的高患病率是由心脏和肾衰竭等潜在疾病以及多种药物和营养不良等因素造成的。全球气温上升也与低钠血症发生率增加有关。慢性低钠血症与跌倒、骨质疏松、骨折、认知和肌肉损伤以及死亡率升高有关。尽管有这些不良后果,但这种情况往往未得到充分诊断和治疗,部分原因是其评估的复杂性。未来指南中简化的分步诊断算法可能有助于解决这一差距。越来越多的证据支持纠正低钠血症的临床益处,促使研究新的治疗方法。其中,SGLT2抑制剂和蛋白质补充剂尤其有希望,不仅在提高血浆钠方面有疗效,而且在提供更广泛的健康益处方面也有疗效。本综述探讨了低钠血症对老年人的影响,总结了其主要原因,并评估了诊断策略以及当前治疗方案的优点和局限性。
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引用次数: 0
Hyponatremia and bone pathophysiology: An integrated preclinical and clinical perspective. 低钠血症和骨病理生理:临床前和临床的综合观点。
Pub Date : 2025-08-29 DOI: 10.1016/j.beem.2025.102028
Emanuele Varaldo, Laura Potasso

Chronic hyponatremia is increasingly recognized as a potential contributor to impaired bone health, although the underlying pathophysiological mechanisms have not yet been fully elucidated. Experimental studies have demonstrated that low serum sodium levels affect both osteoclast and osteoblast function, resulting primarily in increased bone resorption and secondarily in reduced bone formation. In humans, however, evidence regarding the effects of hyponatremia on bone remains limited. Emerging data indicate that acute hyponatremia reduces bone formation activity, while normalization of sodium levels promotes bone formation. These human findings therefore partially differ from preclinical studies, and it remains unclear whether such discrepancies arise from variations in the etiology or severity of hyponatremia in clinical cohorts. In this review, we summarize the current evidence linking both acute and chronic hyponatremia to altered bone metabolism, with a specific focus on the underlying pathophysiological mechanisms and their clinical implications.

慢性低钠血症越来越被认为是骨骼健康受损的潜在因素,尽管其潜在的病理生理机制尚未完全阐明。实验研究表明,低血清钠水平会影响破骨细胞和成骨细胞的功能,主要导致骨吸收增加,其次导致骨形成减少。然而,在人类中,关于低钠血症对骨骼影响的证据仍然有限。新出现的数据表明,急性低钠血症降低骨形成活动,而钠水平正常化促进骨形成。因此,这些人类研究结果与临床前研究存在部分差异,并且尚不清楚这种差异是否源于临床队列中低钠血症的病因或严重程度的差异。在这篇综述中,我们总结了目前将急性和慢性低钠血症与骨代谢改变联系起来的证据,并特别关注其潜在的病理生理机制及其临床意义。
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引用次数: 0
Autoimmune Addison's disease. 自身免疫性艾迪生病。
Pub Date : 2020-01-01 DOI: 10.1056/nejm196312122692422
Serena Saverino, A. Falorni
Primary adrenal insufficiency (PAI) occurs in 1/5000-1/7000 individuals in the general population. Autoimmune Addison's disease (AAD) is the major cause of PAI and is a major component of autoimmune polyendocrine syndrome type 1 (APS1) and type 2 (APS2). Presence of 21-hydroxylase autoantibodies (21OHAb) identifies subjects with ongoing clinical or pre-clinical adrenal autoimmunity. AAD requires life-long substitutive therapy with two-three daily doses of hydrocortisone (HC) (15-25 mg/day) or one daily dose of dual-release HC and with fludrocortisone (0.5-2.0 mg/day). The lowest possible HC dose must be identified according to clinical and biochemical parameters to minimize long-term complications that include osteoporosis and cardiovascular and metabolic alterations. Women with AAD have lower fertility and parity as compared to age-matched healthy controls. Patients must be educated to double-triple HC dose in the case of fever or infections and to switch to parenteral HC in the case of vomiting, diarrhoea or acute hypotension.
原发性肾上腺功能不全(PAI)发生在普通人群中的1/5000-1/7000人中。自身免疫性艾迪生病(AAD)是PAI的主要原因,也是1型(APS1)和2型(APS2)自身免疫性多内分泌综合征的主要组成部分。21羟化酶自身抗体(21OHAb)的存在可识别正在进行临床或临床前肾上腺自身免疫的受试者。AAD需要终身替代治疗,每天两次,三次剂量的氢化可的松(HC)(15-25 mg/天),或每天一次剂量的双效HC和氟氢可的松(0.5-2.0 mg/日)。必须根据临床和生物化学参数确定尽可能低的HC剂量,以最大限度地减少包括骨质疏松、心血管和代谢改变在内的长期并发症。与年龄匹配的健康对照组相比,患有AAD的女性生育能力和生育能力较低。必须教育患者在发烧或感染的情况下将HC剂量增加一倍至三倍,在呕吐、腹泻或急性低血压的情况下改用非肠道HC。
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引用次数: 10
Puberty. 青春期。
Pub Date : 2019-02-15 DOI: 10.1002/9781119386230.ch5
M. Zacharin
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引用次数: 0
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