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Background: Heart failure (HF) is considered an epidemic disease with considerable morbidity, mortality, and immense healthcare costs. Electrolyte abnormalities are often encountered in patients with HF, posing a diagnostic and therapeutic challenge for clinicians. Hyponatremia affects up to one-third of HF patients and represents an unfavorable prognostic factor., Summary: Low sodium levels in HF are mainly attributed to the neurohormonal activation secondary to decreased effective circulating volume. However, patients with HF often have several comorbidities which may cause or exacerbate the preexisting hyponatremia. Factors that provoke HF, such as alcohol overconsumption, may also be involved in hyponatremia development. Furthermore, drugs which are frequently prescribed to HF patients, especially diuretics, are potential culprits of hyponatremia and should always be addressed since their withdrawal may reverse hyponatremia. Despite the great prevalence and deleterious effects of hyponatremia in these patients, it is often overlooked and consequently undertreated. In this review, we present the mechanisms involved in the development of hyponatremia focusing on those besides neurohormonal activation. We also discuss the proper management of this electrolyte disorder which is frequently complex in patients with HF., Key Messages: Hyponatremia in patients with HF is not only the result of neurohormonal activation; several comorbidities and frequently used drugs should also be addressed. Hence, a holistic approach is required both for the diagnosis and optimal treatment., (© 2022 S. Karger AG, Basel.)

Background: Hyponatremia is frequent in acute stroke patients, and it is associated with worse outcomes and increased mortality., Summary: Nonstroke-related causes of hyponatremia include patients' comorbidities and concomitant medications, such as diabetes mellitus, chronic kidney disease, heart failure, and thiazides. During hospitalization, "inappropriate" administration of hypotonic solutions, poor solute intake, infections, and other drugs, such as mannitol, could also lower sodium levels in patients with acute stroke. On the other hand, secondary adrenal insufficiency due to pituitary ischemia or hemorrhage, syndrome of inappropriate antidiuretic hormone secretion, and cerebral salt wasting are additional stroke-related causes of hyponatremia. Although it is yet unclear whether the appropriate restoration of sodium level improves outcomes in patients with acute stroke, the restoration of the volume depletion remains the cornerstone of treatment in hypovolemic hyponatremia. In case of hyper- and euvolemic hyponatremia, apart from the correction of the underlying cause (e.g., withdrawal of an offending drug), fluid restriction, administration of hypertonic solution, loop diuretics, and vasopressin-receptor antagonists (vaptans) are among the therapeutic options. Key Messages: Hyponatremia is frequent in patients with acute stroke. The plethora of underlying etiologies warrants a careful differential diagnosis which should take into consideration comorbidities, concurrent medication, findings from the clinical examination, and laboratory measurements, which in turn will guide management decisions. However, it is yet unclear whether the appropriate restoration of sodium level improves outcomes in patients with acute stroke., (© 2019 S. Karger AG, Basel.)

In clinical practice, several medications such as diuretics, psychotropic drugs, and anticonvulsants have been reported to be a frequent cause of hyponatremia. Drugs may cause hyponatremia either by affecting the homeostasis of sodium and water (e.g., diuretics) or by altering the water homeostasis as a consequence of the syndrome of inappropriate secretion of antidiuretic hormone. On the contrary, drugs commonly prescribed in everyday clinical practice, including proton pump inhibitors, antibiotics, angiotensin-converting enzyme inhibitors, hypoglycemic agents and, amiodarone, have been infrequently 'incriminated' as causes of hyponatremia. Therefore, in the diagnostic approach of patients with low serum [Na+] levels, meticulous history taking and recording of pharmacotherapy is warranted to identify potentially culprit medications. Taking into account the adverse outcomes associated with even mild hyponatremia (i.e., impaired cognition, falls and fractures, mortality), recognition of drug-induced hyponatremia is of vital importance, while responsible agents should be discontinued and "re-challenge" should be avoided by informing the patient and involved caregivers., (© 2019 S. Karger AG, Basel.)

Introduction: Hyponatremia is the most common electrolyte disorder with a prevalence of up to 30% in hospitalized patients. Furthermore, it is associated with increased morbidity and mortality., Areas Covered: This review discusses the efficacy and side effects of the currently available treatment options for hyponatremia and the differences in the pharmacological approach between the European and USA guidelines. Additionally, the authors provide their expert perspectives on current treatment strategies and what they expect from this field in the future., Expert Opinion: Several pharmacological options are available for the treatment of hyponatremia, but data from trials examining and comparing these treatments are missing. Regarding chronic hyponatremia, the role of vaptans should be further analyzed, focusing on comparisons with other active treatments on patient-relevant outcomes and not only on serum sodium concentration. Clinicians should be cautious to an overly rapid increase in serum sodium levels with all available treatment strategies. Finally, it is important to ascertain whether correction of serum sodium levels improves mortality in hyponatremic patients.

Decreased serum sodium concentration is a rather frequent electrolyte disorder in the elderly population because of the presence of factors contributing to increased antidiuretic hormone, the frequent prescription of drugs associated with hyponatremia and also because of other mechanisms such as the "tea and toast" syndrome. The aim of this review is to present certain challenges in the evaluation and treatment of hyponatremia in the elderly population and provide practical solutions. Hyponatremia in elderly subjects is mainly caused by drugs (more frequently thiazides and antidepressants), the syndrome of inappropriate antidiuretic hormone secretion (SIAD) or endocrinopathies; however, hyponatremia is multifactorial in a significant proportion of patients. Special attention is needed in the elderly population to exclude endocrinopathies as a cause of hyponatremia before establishing the diagnosis of SIAD, which then requires a stepped diagnostic approach to reveal its underlying cause. The treatment of hyponatremia depends on the type of hyponatremia. Special attention is also needed to correct serum sodium levels at the appropriate rate, especially in chronic hyponatremia, in order to avoid the osmotic demyelination syndrome. In conclusion, both the evaluation and the treatment of hyponatremia pose many challenges in the elderly population., Competing Interests: Disclosure This review was conducted independently. Professor Elisaf reports personal fees from Astra-Zeneca, grants and personal fees from MSD, personal fees from Pfizer, Abbott, Sanofi-Aventis, Boehringer Ingelheim, Eli-Lilly and GSK. The authors have given talks and attended conferences sponsored by various pharmaceutical companies, including Bristol-Myers Squibb, Pfizer, Lilly, Abbott, Amgen, AstraZeneca, Novartis, Vianex, Teva and MSD. The authors report no other conflicts of interest in this work.

Background: Patients with moderate to severe hypothyroidism and mainly patients with myxedema may exhibit reduced sodium levels (<135 mmol/L)., Summary: The aim of this short review is the presentation of the mechanisms of hyponatremia and of the available data regarding its implications and treatment in patients with hypothyroidism. Hypothyroidism is one of the causes of hyponatremia, thus thyroid-stimulating hormone determination is mandatory during the evaluation of patients with reduced serum sodium levels. The main mechanism for the development of hyponatremia in patients with chronic hypothyroidism is the decreased capacity of free water excretion due to elevated antidiuretic hormone levels, which are mainly attributed to the hypothyroidism-induced decrease in cardiac output. However, recent data suggest that the hypothyroidism-induced hyponatremia is rather rare and probably occurs only in severe hypothyroidism and myxedema. Other possible causes and superimposed factors of hyponatremia (e.g. drugs, infections, adrenal insufficiency) should be considered in patients with mild/moderate hypothyroidism. Treatment of hypothyroidism and fluid restriction are usually adequate for the management of mild hyponatremia in patients with hypothyroidism. Patients with possible hyponatremic encephalopathy should be urgently treated according to current guidelines., Conclusions: Severe hypothyroidism may be the cause of hyponatremia. All hypothyroid patients with low serum sodium levels should be evaluated for other causes and superimposed factors of hyponatremia and treated accordingly., (© 2017 European Society of Endocrinology.)

Hyponatremia (Na(+) <135 mmol/l) is the most common electrolyte disorder. Cirrhosis represents a rather frequent cause of hyponatremia mainly due to systemic and splanchnic vasodilation resulting in decreased effective arterial blood volume, which leads to excessive non-osmotic secretion of antidiuretic hormone. However, hyponatremia of multifactorial origin may be seen in patients with liver diseases. The review focuses on the factors and pathogenetic mechanisms of decreased sodium levels other than the hemodynamic compromise of cirrhosis in patients with liver diseases. The mechanisms and causal or contributing role of pseudohyponatremia, hyperglycemia, infections, drugs and toxins as well as of endocrine disorders, renal failure and cardiac disease in patients with liver disease are meticulously discussed. Hyponatremia of multifactorial origin is frequently observed in patients with liver diseases, and special efforts should be made to delineate the underlying causative and precipitating factors as well as the risk factors of the osmotic demyelination syndrome in order to properly manage this serious electrolyte disorder and avoid treatment pitfalls.

Hyponatremia (serum sodium <135 mEq/L) is a common electrolyte disorder in community or hospitalized patients. Serum sodium levels should be corrected at a proper rate in patients with hyponatremia, since overcorrection of serum sodium levels is related to devastating neurologic consequences, such as the osmotic demyelination syndrome (ODS). However, a number of pitfalls, which could lead to undercorrection or overcorrection of hyponatremia, are common during the treatment of hyponatremic patients. Hereby, we describe ten common pitfalls that are observed during the correction of serum sodium concentration in hyponatremic patients. These refer to pitfalls in the goals and limits of the correction rate of serum sodium, pitfalls in the means (e.g. solutions but also drugs) and formulas used for achieving the desired correction rate and pitfalls associated with inadequate management or overcorrection. The knowledge of these common-in-clinical-practice pitfalls could assist clinicians in the proper management of patients with hyponatremia.

Hyponatremia is the most common electrolyte disorder in hospitalized patients associated with increased morbidity and mortality. On the other hand, inappropriate treatment of hyponatremia (under- or mainly overtreatment) may also lead to devastating consequences. The appropriate diagnosis of the causative factor is of paramount importance for the proper management and avoidance of treatment pitfalls. Herein, we describe the most common pitfalls in the evaluation of the hyponatremic patient, such as failure to exclude pseudohyponatremia or hypertonic hyponatremia (related to glucose, mannitol or glycine), to properly assess urine sodium concentration and other laboratory findings, to diagnose other causes of hyponatremia (cerebral salt wasting, reset osmostat, nephrogenic syndrome of inappropriate antidiuresis, prolonged strenuous exercise, drugs) as well as inability to measure urine osmolality or delineate the diagnosis and cause of the syndrome of inappropriate antidiuretic hormone secretion. Clinicians should be aware of these common clinical practice pitfalls, which could endanger patients with hyponatremia., (Copyright © 2015 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.)

Hyponatremia is the most common electrolyte disorder and is associated with serious neurologic sequelae and increased mortality. Conventional treatment options for hyponatremia, such as fluid restriction, hypertonic saline, loop diuretics, demeclocycline or urea, are ineffective in the long-term. The present review considers the role of vasopressin receptor inhibitors (vaptans), focusing on lixivaptan, in the treatment of patients with euvolemic or hypervolemic hyponatremia. Lixivaptan is an oral selective V2 receptor inhibitor, which produces a significantly greater increase of serum sodium levels compared with placebo. These effects seem promising, but more trials are needed to examine whether the beneficial effect of lixivaptan on serum sodium concentration translates into clinical benefit in these patient populations.

Hyponatremia is a common electrolyte disturbance associated with considerable morbidity and mortality. Hyponatremia may not infrequently be present during the course of an infection, does not cause specific symptoms and may be overlooked by clinicians. Nonetheless, it may reflect the severity of the underlying process. This review focuses on the clinical and pathophysiological aspects of hyponatremia associated with infectious diseases. In the majority of cases, the fall in serum sodium concentration is of multifactorial origin owing to increased secretion of the anti-diuretic hormone either appropriately or inappropriately. Inadvertent administration of fluids may worsen hyponatremia and prolong morbidity., (Copyright © 2011 The British Infection Association. Published by Elsevier Ltd. All rights reserved.)

Hyponatremia is the most common electrolyte disorder and is mainly known for its neurological complications. New studies suggest previously unrecognized complications of hyponatremia, including falls, osteoporosis and fractures. Because these novel associations are mainly derived from epidemiological studies, it remains unclear whether hyponatremia has a direct effect on bone or whether it is a surrogate marker of another etiology. However, one animal and one in vitro study now show that hyponatremia can have direct effects on bone, mainly via activation of osteoclasts. The association between hyponatremia and fractures appears to be independent of osteoporosis (defined as low BMD). Also, data suggest that this association cannot be fully explained by the possibility that hyponatremia predisposes to falls. Hyponatremia, therefore, also has an effect on bone quality that is not captured by BMD. Here, the emerging relationship between hyponatremia and bone is reviewed, with special emphasis on possible mechanisms, unanswered questions and clinical implications.

Hyponatremia is a common electrolyte abnormality with the potential for significant morbidity and mortality. Endocrine disorders, including adrenal deficiency and hypothyroidism, are uncommon causes of hyponatremia. Primary adrenal insufficiency (i.e. Addison's disease) may well be recognized by clear hall-marks of the disease, such as pigmentation, salt craving, hypotension, and concomitant hyperkalemia. Addison's disease is an important diagnosis not to be missed since the consequences can be grave. On the other hand, hypothyroidism and secondary adrenocortical insufficiency originating from diseases of the hypothalamus and/or pituitary (hypopituitarism) require a high index of suspicion, because the clinical signs can be quite subtle. This review focuses on clinical and pathophysiological aspects of hyponatremia due to endocrine disorders.

Hyponatremia (defined as a serum sodium level < 134 mmol/L) is the most common electrolyte abnormality in hospitalized patients. Certain drugs (eg, diuretics, antidepressants, and antiepileptics) have been implicated as established causes of either asymptomatic or symptomatic hyponatremia. However, hyponatremia occasionally may develop in the course of treatment with drugs used in everyday clinical practice (eg, newer antihypertensive agents, antibiotics, and proton pump inhibitors). Physicians may not always give proper attention in time to undesirable drug-induced hyponatremia. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on serum sodium levels. Here, we review clinical information about the incidence of hyponatremia associated with specific drug treatment and discuss the underlying pathophysiologic mechanisms.

Background: Diuretics are one of the most common causes of severe hyponatremia. The responsible pathogenetic mechanisms remain unclear. Serum uric acid concentration has been proposed as an index of differentiating between two pathophysiologic constructs of diuretic-induced hyponatremia-extracellular volume depletion and syndrome of inappropriate antidiuretic hormone secretion (SIADH)-like state-but its discriminating value has not been verified in large series of patients. Here we attempt to illuminate the pathophysiology of diuretic-induced hyponatremia by focusing on uric acid homeostasis. Additionally, we analyze the epidemiology and clinical characteristics of the disorder., Methods: We studied prospectively 158 adult patients with hyponatremia on admission to our internal medicine clinic. Here we report on those with diuretic-induced hyponatremia., Results: Forty patients (13 male and 27 female) had diuretic-induced hyponatremia, rendering it the most common cause of the disorder (25.3%). These patients had lower mean ([Na+]) (121.2 +/- 7.2 vs 126.4 +/- 4.1 mEq/L, p = .0001) than the remaining hyponatremic patients. Patients with serum uric acid levels < 4 mg/dL (n = 14) exhibited a biochemical profile consistent with a SIADH-like state, whereas patients with serum uric acid levels > or = 4 mg/d (n = 26) were consistent with extracellular volume depletion., Conclusions: Diuretics are the most common cause of community-developed hyponatremia. The serum uric acid level effectively discriminates between two biochemical profiles of diuretic-induced hyponatremia, one consistent with extracellular volume depletion and another that simulates SIADH.

Object: Electrolyte abnormalities are frequently observed in patients with hyponatremia. The aim of this study was to determine the incidence of various electrolyte abnormalities encountered in hyponatremic patients admitted to an internal medicine clinic, as well as to investigate the possible pathogenetic mechanisms responsible for these abnormalities., Patients and Methods: We prospectively studied 204 adult patients who either on admission to our clinic or during their hospitalization were found to have hyponatremia., Results: Ninety-two patients (45.5%) had at least one additional electrolyte abnormality. Hypophosphatemia was the most frequent electrolyte disorder observed (35 patients, 17%). Hypokalemia was seen in 32 patients (15.8%), hypomagnesemia in 31 patients (15.2%) and hyperkalemia in 12 patients (5.9%). Moreover, 5 patients (2.5%) had hyperphosphatemia, 4 patients (1.9%) exhibited hypermagnesemia, 3 patients (1.4%) had hypercalcemia, and 6 patients (2.9%) had true hypocalcemia. There were no statistically significant differences regarding the incidence of these electrolyte abnormalities (as a whole) between the main subgroups of hyponatremic patients (diuretic-induced, syndrome of inappropriate antidiuretic hormone, hypovolemia-induced and edematous state-related). However, hypokalemia and hypomagnesemia were more frequently observed in patients with diuretic-induced hyponatremia, while hyperkalemia was more frequently seen in edematous state-related hyponatremia., Conclusions: Additional electrolyte abnormalities are frequently encountered in patients with hyponatremia of any origin admitted to an internal medicine clinic.

The syndrome of inappropriate ADH secretion (SIADH) is a common cause of hyponatremia. However, other metabolic abnormalities have infrequently been described in patients with the syndrome of inappropriate antidiuresis. Here, we describe a female patient with hyponatremia due to SIADH who presented with a cluster of metabolic abnormalities and specifically hypouricemia associated with uricosuria, hypokalemia caused by renal potassium wasting, hypomagnesemia with inappropriate magnesiuria, hypophosphatemia with renal phosphate wasting and inappropriate calciuria. These abnormalities could be partly due to the extracellular volume expansion and were corrected with the water restriction-induced increase in serum sodium levels., (Copyright 2002 S. Karger AG, Basel)

Hyponatraemia is commonly reported in chronic alcoholic patients. However, the underlying pathogenetic mechanisms are not well delineated. In the current study, we analysed the possible pathophysiological mechanisms of hyponatraemia in a group of alcoholic patients (n = 127) admitted to our hospital for causes related to alcohol misuse. Hyponatraemia (serum sodium <134 mmol/l) was found in 22 patients (17.3%). The most common cause of hyponatraemia in our cohort was hypovolaemia (12 patients); pseudohyponatraemia was diagnosed in six patients with alcohol-induced severe hypertriglyceridaemia. It is of interest that two patients fulfilled the criteria of the so-called 'beer potomania' syndrome, while in two others, hyponatraemia was due to reset osmostat or to cerebral salt wasting syndrome, not previously described in alcoholic patients. It is concluded that hyponatraemia is a frequently observed electrolyte disorder in hospitalized alcoholic patients and is related to various pathophysiological mechanisms.

Even though many disorders of the nervous system have been reported to be associated with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), the association of this syndrome with multiple sclerosis is extremely rare. We describe a patient with multiple sclerosis who developed SIADH and hyponatremia.

Background: Patients with moderate to severe hypothyroidism and mainly patients with myxedema may exhibit reduced sodium levels (<135 mmol/L). Summary: The aim of this short review is the presentation of the mechanisms of hyponatremia and of the available data regarding its implications and treatment in patients with hypothyroidism. Hypothyroidism is one of the causes of hyponatremia, thus thyroid-stimulating hormone determination is mandatory during the evaluation of patients with reduced serum sodium levels. The main mechanism for the development of hyponatremia in patients with chronic hypothyroidism is the decreased capacity of free water excretion due to elevated antidiuretic hormone levels, which are mainly attributed to the hypothyroidism-induced decrease in cardiac output. However, recent data suggest that the hypothyroidism-induced hyponatremia is rather rare and probably occurs only in severe hypothyroidism and myxedema. Other possible causes and superimposed factors of hyponatremia (e.g. drugs, infections, adrenal insufficiency) should be considered in patients with mild/moderate hypothyroidism. Treatment of hypothyroidism and fluid restriction are usually adequate for the management of mild hyponatremia in patients with hypothyroidism. Patients with possible hyponatremic encephalopathy should be urgently treated according to current guidelines. Conclusions: Severe hypothyroidism may be the cause of hyponatremia. All hypothyroid patients with low serum sodium levels should be evaluated for other causes and superimposed factors of hyponatremia and treated accordingly. [ABSTRACT FROM AUTHOR]