Pub Date : 2025-10-08DOI: 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.
{"title":"Diagnostic algorithm of hyponatremia.","authors":"Rose Lin, Mathis Grossmann, Annabelle M Warren","doi":"10.1016/j.beem.2025.102053","DOIUrl":"https://doi.org/10.1016/j.beem.2025.102053","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":93894,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":" ","pages":"102053"},"PeriodicalIF":0.0,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145294625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-26DOI: 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.
{"title":"Special considerations of hyponatremia in the elderly patient.","authors":"Julie Refardt","doi":"10.1016/j.beem.2025.102040","DOIUrl":"https://doi.org/10.1016/j.beem.2025.102040","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":93894,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":" ","pages":"102040"},"PeriodicalIF":0.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145282195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-29DOI: 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.
{"title":"Hyponatremia and bone pathophysiology: An integrated preclinical and clinical perspective.","authors":"Emanuele Varaldo, Laura Potasso","doi":"10.1016/j.beem.2025.102028","DOIUrl":"https://doi.org/10.1016/j.beem.2025.102028","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":93894,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":" ","pages":"102028"},"PeriodicalIF":0.0,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-01DOI: 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.
{"title":"Autoimmune Addison's disease.","authors":"Serena Saverino, A. Falorni","doi":"10.1056/nejm196312122692422","DOIUrl":"https://doi.org/10.1056/nejm196312122692422","url":null,"abstract":"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.","PeriodicalId":93894,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":"1 1","pages":"101379"},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1056/nejm196312122692422","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42725642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}