Refractory hyponatremia in neuromyelitis optica in a pediatric patient: A case report.

RATIONALE: Neuromyelitis optica spectrum disorders (NMOSD) is a rare autoimmune disease predominantly involving optic nerves and spinal cord, and possible comorbidities including syndrome of inappropriate antidiuretic hormone secretion or urinary complication. We reported a young girl diagnosed with NMOSD presented with refractory hyponatremia, acute urine retention, and general weakness. Clinical symptoms improved gradually after receiving intravenous immunoglobulin, high-dose methylprednisolone, and plasmapheresis. NMOSD should be kept in mind in adolescence with acute urine retention, intermittent fever, and hyponatremia. PATIENT CONCERNS: A 15-year-old girl admitted to our hospital due to no urination for 2 days. DIAGNOSIS: Aquaporin-4 antibodies were detected showing positive both in serum and cerebrospinal fluid. Long transverse myelitis in cervical and thoracic spinal cord and optic neuritis was revealed in magnetic resonance imaging. INTERVENTIONS: Intravenous immunoglobulin 2 g/kg was infused totally in 4 days, and methylprednisolone pulse therapy was subsequently followed in 5 days; followed by 5 courses of plasmapheresis a week later. OUTCOMES: Her muscle power, syndrome of inappropriate antidiuretic hormone secretion condition, and urinary function were all improved after immune-modulated treatment course; NMOSD relapsed twice within the first year after diagnosis, however no relapse of NMOSD in the subsequent 1 year. LESSONS: To the best of our knowledge, this was the first childhood case of NMO accompanied by refractory hyponatremia in the reported literature. In childhood cases presenting with refractory hyponatremia and limb weakness, NMO or NMOSD should be considered possible diagnoses despite their rarity in pediatric cases.

Hyponatremia in heart failure.

Hyponatremia is one of the newer and emerging risk factors for an adverse prognosis in chronic heart failure. Why decreased serum sodium is associated with worse prognosis remains unclear. It may reflect worsening heart failure and the deleterious effects of activation of neurohormones. The mechanism of hyponatremia in heart failure also remains unclear. A relatively greater degree of free-water retention compared to sodium retention is probably the major mechanism. The treatment of significant hyponatremia in heart failure is difficult. The conventional treatments such as fluid restriction, infusion of hypertonic saline, and aggressive diuretic therapies are not usually effective. Vasopressin receptor antagonists have been shown to enhance aquaresis and correct hyponatremia. However, long-term beneficial effects of such treatments in chronic heart failure have not been documented.

Sensitivity of International Classification of Diseases codes for hyponatremia among commercially insured outpatients in the United States.

BACKGROUND: Administrative claims are a rich source of information for epidemiological and health services research; however, the ability to accurately capture specific diseases or complications using claims data has been debated. In this study, the authors examined the validity of International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) diagnosis codes for the identification of hyponatremia in an outpatient managed care population. METHODS: We analyzed outpatient laboratory and professional claims for patients aged 18 years and older in the National Managed Care Benchmark Database from Integrated Healthcare Information Services. We obtained all claims for outpatient serum sodium laboratory tests performed in 2004 and 2005, and all outpatient professional claims with a primary or secondary ICD-9-CM diagnosis code of hyponatremia (276.1). RESULTS: A total of 40,668 outpatient serum sodium laboratory results were identified as hyponatremic (serum sodium < 136 mmol/L). The sensitivity of ICD-9-CM codes for hyponatremia in outpatient professional claims within 15 days before or after the laboratory date was 3.5%. Even for severe cases (serum sodium < or = 125 mmol/L), sensitivity was < 30%. Specificity was > 99% for all cutoff points. CONCLUSION: ICD-9-CM codes in administrative data are insufficient to identify hyponatremia in an outpatient population.

Recognition and treatment of hyponatremia in acutely ill hospitalized patients.

OBJECTIVE: The objective of this paper was to discuss the diagnosis, pathophysiology, and management of hyponatremia among critically ill, hospitalized patients (eg, after surgery or in the intensive care unit). METHODS: English-language literature published between 1967 and 2006 was searched using several key words (AVP receptor antagonists, hyponatremia, SIADH, conivaptan, tolvaptan, and lixivaptan) and by accessing MEDLINE and ScienceDirect. Meeting abstracts from scientific sessions (American Society of Nephrology Renal Week 2004 and the Endocrine Society's 87th Annual Meeting [2005]) were reviewed. The package insert for conivaptan hydrochloride injection was referenced from . Clinical trials included in this review were randomized and placebo controlled. RESULTS: Based on the literature we researched, hyponatremia is the most common electrolyte disorder encountered in critical care and is associated with a variety of conditions, including congestive heart failure and the syndrome of inappropriate antidiuretic hormone secretion. Because hyponatremia can arise in hypervolemic, euvolemic, and hypovolemic states, clinicians may not recognize its presence and cause. Incorrect management can lead to significant morbidity and mortality. Physicians need to recognize risk factors and symptoms and use appropriate treatment guidelines for hyponatremia. Traditionally, therapy for hyponatremia has been limited by efficacy and safety concerns. Arginine vasopressin (AVP) receptor antagonists, therapeutic agents that promote aquaresis in patients with hyponatremia by targeting V(1a) receptors in the vascular smooth muscle, V(2) receptors in the kidney, or both, are under development. A dual-receptor antagonist targeting both V(1a) and V(2) receptors is now approved for the treatment of euvolemic hyponatremia in hospitalized patients. CONCLUSIONS: Hyponatremia, an electrolyte abnormality found in critically ill patients, can be associated with significant morbidity and mortality. AVP receptor antagonists show promise as effective and tolerable treatments for patients with hyponatremia.

Management of hyponatremia and clinical use of vasopressin antagonists.

Hyponatremia, the most common electrolyte disorder in hospitalized patients, has been associated with high rate of mortality among both this population and nonhospitalized patients. This review describes briefly the classification and pathogenesis of hyponatremia, and, in greater detail, the management of hyponatremia with a particular emphasis on the clinical pharmacology of arginine vasopressin (AVP) antagonists. This review includes more in-depth discussion on the pharmacology of conivaptan, an AVP antagonist recently approved by the United States Food and Drug Administration.

Hyponatraemia in clinical practice.

Hyponatraemia is defined as a serum sodium concentration below 135 mmol/l. It causes major diagnostic and management problems in practice. Hyponatraemic disorders are divided into euvolaemic, hypervolaemic and hypovolaemic. In the evaluation of the hyponatraemic patient, history taking should focus on identifying the potential cause, duration and symptomatology. Clinical examination should include assessment of volume status. Acute hyponatraemia of less than 48 h duration requires prompt correction. Treatment may involve hypertonic saline, isotonic saline and appropriate hormone replacement therapy depending on the aetiology. Chronic hyponatraemia should be treated with caution because of the risk of central pontine myelinolysis.

Current issues for nurse practitioners: Hyponatremia.

PURPOSE: To review the assessment, diagnosis, and management of hyponatremia (serum sodium <135 mEq/L), the most common electrolyte disturbance as a result of dysregulation of water balance in hospitalized or institutionalized patients. DATA SOURCES: Comprehensive search using keywords AVP receptor antagonists, hyponatremia, SIADH, conivaptan, tolvaptan, lixivaptan, nurse practitioner, and others was carried out using the National Library of Medicine (PubMed) Web site from which full-text articles were obtained. Meeting abstracts were obtained from scientific sessions including the American Society of Nephrology Renal Week 2004 and the Endocrine Society's 87th Annual Meeting (2005). The Vaprisol (conivaptan hydrochloride injection) package insert was referenced and obtained from FDA.gov. CONCLUSIONS: A diagnosis of hyponatremia requires thorough investigation for underlying causes and prompt treatment to prevent poor patient outcomes. In clinical trials, a new class of drugs called the arginine vasopressin (AVP) receptor antagonists or aquaretics has been shown to be safe and effective for the treatment of hyponatremia. Among this class of agents, intravenous conivaptan hydrochloride, indicated for the treatment of euvolemic hyponatremia in hospitalized patients, is the first drug in class approved for use. IMPLICATIONS FOR PRACTICE: Elderly patients, and those with certain conditions such as heart failure, tuberculosis, cirrhosis, and head injury, may be at increased risk for hyponatremia. In hospitalized patients following surgery and the use of certain medications, hyponatremia is a common condition. A thorough understanding of the physiology of water balance and the risk factors associated with hyponatremia is essential for prompt and effective intervention. Awareness of the limitations of conventional therapies and the availability of new treatment options for hyponatremia allows clinicians to optimize patient care.

Hyponatremia, fluid-electrolyte disorders, and the syndrome of inappropriate antidiuretic hormone secretion: diagnosis and treatment options.

OBJECTIVE: To review the types and causes of hyponatremia and examine the various strategies for treatment of this disorder. METHODS: A systematic review of the current literature is provided, targeting endocrinology clinicians who consult with hospital medical and surgical staff when managing patients with hyponatremia. Treatment for euvolemic and hypervolemic hyponatremia with arginine vasopressin receptor antagonists is presented, which provides a new treatment option for patients with disorders of water metabolism. RESULTS: Hyponatremia is recognized as the most common electrolyte disorder encountered in the clinical setting and is associated with a variety of conditions including dilutional disorders, such as congestive heart failure and the syndrome of inappropriate antidiuretic hormone secretion, and depletional disorders, such as diarrhea and vomiting or blood loss. Most cases of mild hyponatremia can be treated effectively. Acute, severe hyponatremia that is untreated or treated ineffectively, however, can lead to serious neurologic outcomes or death. With the poor prognosis for morbidity and mortality in patients with severe hyponatremia, hospital-based clinicians must identify those at risk for hyponatremia and suggest appropriate treatment intervention. A new class of drugs, the arginine vasopressin receptor antagonists, targets receptors on collecting duct cells of the nephron and causes aquaresis, the excretion of free water. This therapy leads to the restoration of sodium-water homeostasis in patients with euvolemic and hypervolemic hyponatremia. CONCLUSION: With many hospitalized patients at risk for hyponatremia, especially elderly patients in critical care and postsurgical units, identification of involved patients, recommendation of appropriate treatment, and awareness of new therapeutic options are critical.

Hyponatremia: why it matters, how it presents, how we can manage it.

Hyponatremia is a common electrolyte disorder among hospitalized patients and has been associated with increased mortality. Most patients are asymptomatic, but many do present with symptoms, usually of a generalized neurologic nature. Based-on medical history, physical examination (including volume-status assessment), and laboratory tests, patients can be classified as having either hypervolemic, euvolemic, or hypovolemic hyponatremia. Management depends on the speed of hyponatremia onset; its degree, duration, and symptoms; and whether there are risk factors for neurologic complications. The risks of overly rapid correction must be weighed against the benefits of treating hyponatremia. Traditional therapies have significant limitations. New agents that antagonize arginine vasopressin at the V2 receptor or both the V(1A) and V2 receptors show promise for treating hypervolemic and euvolemic hyponatremia, as they induce desired free water diuresis without inducing sodium excretion.

Disorders of water imbalance.

Disorders of water imbalance manifest as hyponatremia and hypernatremia. To diagnose these disorders, emergency physicians must maintain a high index of suspicion, especially in the high-risk patient, because clinical presentations may be nonspecific. With severe water imbalance, inappropriate fluid resuscitation in the emergency department may have devastating neurological consequences. The rate of serum sodium concentration correction should be monitored closely to avoid osmotic demyelination syndrome in hyponatremic patients and cerebral edema in hypernatremic patients.

Inpatient hyponatraemia: adequacy of investigation and prevalence of endocrine causes.

This study assessed the effect of endocrine input on the investigation of hyponatraemia and examined the prevalence of endocrine causes of hyponatraemia. This single-centre, retrospective study included 139 inpatients (median age, 74 years) with serum sodium (Na) levels ≤128 mmol/l during hospitalisation at a UK teaching hospital over a three-month period. In total, 61.9% of patients underwent assessment of volume status and 28.8% had paired serum and urine osmolality, and Na measured. In addition, 14.4% of patients received endocrine input; 80% of these patients underwent full work-up of hyponatraemia compared with 5% of patients not referred to endocrine services (p < 0.001; relative risk, 15.86; 95% confidence interval, 7.17-31.06). The prevalence of adrenal insufficiency was 0.7%, but basal serum cortisol levels were not measured in around two-thirds of patients. Despite 26.7% of patients having abnormal thyroid function tests, no patient was diagnosed with severe hypothyroidism. More widespread provision of expert input should be considered.

Chronic idiopathic hyponatremia in older people due to syndrome of inappropriate antidiuretic hormone secretion (SIADH) possibly related to aging.

OBJECTIVE: To determine the prevalence of syndrome of inappropriate antidiuretic hormone secretion (SIADH) among older hyponatremic patients in a subacute geriatric facility, to identify patients with no apparent cause for the SIADH (idiopathic SIADH), and to determine their clinical characteristics. DESIGN: Prospective analysis of a cohort of older patients over a period of 3 months. SETTING: Two wards in a geriatric rehabilitation hospital. PARTICIPANTS: Patients aged 65 and older. MEASUREMENTS: All patients with hyponatremia (serum sodium <135 mmols/l) were clinically examined and relevant investigations were performed to determine the etiology of hyponatremia. Patients were observed for symptoms of hyponatremia. Hyponatremia was classified into possible SIADH and non-SIADH types. Patients with SIADH type hyponatremia were screened for possible causes. Past medical histories were obtained from the general practitioners. RESULTS: Of the 172 patients studied, 43 (25%) had hyponatremia. It was symptomatic in only four patients. Twenty-two (51%) had SIADH etiology. In nine (mean age 84 +/- 4), no cause for the SIADH was evident (presumed idiopathic SIADH) and in seven, hyponatremia (128-135 mmols/l) was chronic (12 to 72 months). Further reduction in serum sodium, which was symptomatic, was noted in two of these patients with the onset of pneumonia. CONCLUSION: Most older hyponatremic patients in a rehabilitation setting seem to have SIADH etiology. This study confirms the presence of a group of older individuals with chronic idiopathic hyponatremia in whom the underlying mechanism may be SIADH related to aging. Hyponatremia is modest in these patients and has little clinical significance. However, they may be at increased risk of developing symptomatic hyponatremia with intercurrent illnesses.

Intranasal desmopressin-induced hyponatremia.

Desmopressin is a commonly used, well-tolerated agent for the treatment of primary nocturnal enuresis and central diabetes insipidus. Intranasal desmopressin provides symptomatic relief with few serious complications. A 29-year-old woman with a long history of primary nocturnal enuresis began treatment with intranasal desmopressin. Although the enuresis ceased, she developed throbbing headaches, nausea, vomiting, paresthesia, lethargy, fatigue, and altered mental status over the next 7 days. When she came to the emergency room her sodium concentration was 127 mmol/L. The history of desmopressin use was not obtained at that time. She was treated with intravenous fluids and discharged. The symptoms returned and worsened over the next 4 days, and she returned to the emergency room stuporous. A repeat sodium was 124 mmol/L, and she was admitted. The history of desmopressin use was still not available. Medical evaluations included computerized tomography, lumbar puncture, complete blood counts, serum chemistries, and serologies. The next morning the woman was improved and informed clinicians of her desmopressin use. Without other causes for the hyponatremia, she was diagnosed with the syndrome of inappropriate antidiuretic hormone, presumably caused by desmopressin. Within 24 hours of fluid restriction and cessation of desmopressin, her symptoms and hyponatremia resolved. A review of the literature found 11 children and 2 adults in whom intranasal desmopressin was associated with hyponatremia, all of whom experienced seizures or altered mental status. Our patient illustrates the importance of early recognition and treatment of hyponatremia before the onset of seizures. When vague symptoms develop during desmopressin therapy, hyponatremia must be considered as part of the differential diagnosis. It may also be prudent to screen for electrolyte abnormalities in patients taking this agent to prevent serious iatrogenic complications.

Hyponatremia in the neurosurgical patient: diagnosis and management.

Hyponatremia is frequently encountered in patients who have undergone neurosurgery for intracranial processes. Making an accurate diagnosis between the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting (CSW) in patients in whom hyponatremia develops is important because treatment differs greatly between the conditions. The SIADH is a volume-expanded condition, whereas CSW is a volume-contracted state that involves renal loss of sodium. Treatment for patients with SIADH is fluid restriction and treatment for patients with CSW is generally salt and water replacement. In this review, the authors discuss the differential diagnosis of hyponatremia, distinguish SIADH from CSW, and highlight the diagnosis and management of hyponatremia, which is commonly encountered in patients who have undergone neurosurgery, specifically those with traumatic brain injury, aneurysmal subarachnoid hemorrhage, recent transsphenoidal surgery for pituitary tumors, and postoperative cranial vault reconstruction for craniosynostosis.

Hyponatremic dehydration: an analysis of 78 cases.

Our purpose was to determine the frequency of convulsion in children with hyponatremic dehydration (HD). We also investigated whether or not there was a relationship between the severity of hyponatremia and the degrees of malnutrition in our region (Eastern Anatolia of Turkey) in where malnutrition is frequently observed. In this study, the clinical and laboratory findings of 78 patients with diarrhoea (acute, persistent or chronic diarrhoea) and HD were studied. When diarrhoea lasts longer than 2 and 4 weeks they were accepted as persistent and chronic diarrhoea, respectively. Patients were said to have HD if they had the clinical findings of dehydration associated with hyponatremia [Serum sodium (SNa) <130 mmol/L)]. Nutritional status of the children was assessed by the Gomez classification using weight for age; it was accepted as normal those were between 90%-110%, mild malnutrition 75%-89%, moderate malnutrition 60%-74% and severe malnutrition <60%. Of 78 patients, 40 were boys, 38 were girls. The age and weight of the patients ranged from 40 days to 36 months (8.94 +/- 5.49 months) and from 2000 to 10,300 g (5535.25 +/- 1702.10 g) respectively. All patients except four had malnutrition; 15 (20.3%) had mild malnutrition, 30 (40.5%) had moderate malnutrition and 29 (39.2%) had severe malnutrition. Forty-seven patients had acute, 16 patients had persistent, and 15 patients had chronic diarrhoea. SNa levels were between 104 and 129 mmol/L (121.21 +/- 6.12 mmol/L). There was not statistically a significant difference between SNa level and the degree of malnutrition, and SNa level and the types (acute, persistent or chronic) of diarrhoea (p > 0.05). Of 78 patients, 12 (15.3%) patients had convulsion, of whom eight had convulsion associated with fever. Convulsion was noted in nine (19.1%) and three (18.7%) patients with acute and persistent diarrhoea, respectively (p > 0.05). Also, we observed that when hyponatremia was severer, convulsions tended to be more occuring (p < 0.05). Five (6.4%) children died and all of them had severe malnutrition and septicemia. We determined that the frequency of convulsion in HD was 15.3% (12/78), and there was not a difference between the cases of acute, persistent and chronic diarrhoea for the frequency of convulsion. We also found a significant difference was not present between SNa level and the degree of malnutrition, and between SNa level and the types (acute, persistent or chronic) diarrhoea. However, we observed that when hyponatremia was severer, convulsions tended to be more occuring.

[Incidence, causes and prognostic factors of hyponatremia in intensive care]. / Incidence, étiologies et facteurs pronostiques de l'hyponatrémie en réanimation.

PURPOSE: The incidence of hyponatremia is unknown, their causes are multiple. The higher mortality, especially in intensive care units, is currently unexplained. The objective of this article is to evaluate the incidence of hyponatremia, to assess their causes and to identify predictors of prognosis in intensive care units. METHODS: We included retrospectively all patients admitted at department of medical intensive care unit between January 1996 and February 2001, who presented at the admission, an hyponatremia (< 130 mmol/l). We excluded all patients who presented a hospital acquired hyponatremia, or hyponatremia associated with hyperglycemia > 13 mmol/l or with mannitol administration. Data were analysed by univariate methods, then by multivariate analysis. RESULTS: During the study period, 300 patients were identified among 2188: the incidence was 13.7% with 95% confidence interval (95% CI) between 9.8 % and 16.7%. Hypovolemic hyponatremia was observed in 25.7%, hypervolemic in 23.7% and normovolemic in 50.6%. In-hospital mortality was 37.7% (95% CI: 31.8% - 42.3%). Nine data were significantly associated with higher mortality in univariate analysis, but only 5 were identified as independant predictors of hospital mortality in multivariate analysis: hyponatremia < 125 mmol/l with a significant relative risk (RR) (RR = 2.10; 95% CI: 1.43-3.08; p < 0.001), Glasgow score < 9 (RR = 2.66; 95% CI: 1.25-5.66; p = 0.01), Glasgow score between 9 and 14 (RR = 1.94; 95% CI: 1.31-2.88; p < 0.001), shock (RR = 1.80; 95% CI: 1.10-3.05; p = 0.02) and blood urea concentration > 10 mmol/l (RR = 1.59; 95% CI : 1.08-2.34; p = 0.02). CONCLUSION: The frequency of hyponatremia is high; the normovolemic type represented 50%. Mortality is linked, in greater part, to organs dysfunction, but the severity of hyponatremia remained a significant predictor of mortality.

[Treatment of severe hyponatremia (<120mEq/l)]. / Traitement d'une hyponatrémie sévère (< 120 mEq/l).

Inadequate treatment of severe hyponatremia (< 120 mEq/l) can be associated with severe neurological damage. Acute hyponatremia (< 48 h) is usually observed in the postoperative period, these patients need prompt treatment with hypertonic saline (3%) to avoid epilepsia and respiratory arrest. Patients with chronic symptomatic hyponatremia (> 48-72 h) need a rapid correction of SNa the first hours (to decrease brain oedema) followed by a slow correction so that the daily increase in SNa stay under 10 mEq/l/24 h, to avoid the "Osmotic Demyelinating Syndrome" (ODS). Patients with asymptomatic hyponatremia need a slow correction. In patients who are overtreated, decreasing the SNa by giving hypotonic solutions (eventually with DDAVP) so that the daily increase in SNa stays under 10 mEq/l/24 h could protect them again ODS. Frequent measurements of SNa during the correction phase of SNa are mandatory to avoid overcorrection. The use of urea for the management of hyponatremia could represent a good alternative to hypertonic saline. In animals, urea treatment has been clearly shown to protect again ODS, this protective effect could be due to its ability to induce quickly brain "organic osmolytes" reaccumulation.

Hyponatremia: pathophysiology, classification, manifestations and management.

Hyponatremia has complex pathophysiology, is frequent and has potentially severe clinical manifestations, and its treatment is associated with high risks. Hyponatremia can be hypertonic, isotonic or hypotonic. Hypotonic hyponatremia has multiple etiologies, but only two general mechanisms of development, defective water excretion, usually because of elevated serum vasopressin levels, or excessive fluid intake. The acute treatment of symptomatic hypotonic hyponatremia requires understanding of its targets and risks and requires continuous monitoring of the patient's clinical status and relevant serum biochemical values. The principles of fluid restriction, which is the mainstay of management of all types of hypotonic hyponatremia, should be clearly understood and followed. Treatment methods specific to various categories of hyponatremia are available. The indications and risks of these treatments should also be well understood. Rapid correction of chronic hypotonic hyponatremia may lead to osmotic demyelination syndrome, which has severe clinical manifestations, and may lead to permanent neurological disability or death. Prevention of this syndrome should be a prime concern of the treatment of hypotonic hyponatremia.

Hyponatremia caused by polydipsia.

Hyponatremia (serum sodium <135 mEq/L) is the most common electrolyte disorder. The severity of symptoms is related to how rapidly the condition develops and the degree of cerebral edema that results from the low serum level of sodium. Hypertonic saline and the new vasopressin receptor antagonists are highly effective treatments for severe symptomatic hyponatremia, yet they can result in severe neurological complications if sodium levels are restored too quickly. Hyponatremia is classified as hypovolemic, euvolemic, and hypervolemic. Treatments include administration of high-risk medications and fluid restriction to restore fluid and electrolyte balance and relieve cerebral effects. Nursing care to ensure safe outcomes involves multidisciplinary collaboration, close monitoring of serum sodium levels and intake and output, and assessment for neurological changes.

[Hyponatremic syndrome]. / Sindrome iponatriemica.

Sodium, the most important extracellular fluid electrolyte, is the focus of several homeostatic mechanisms that regulate fluid and electrolyte balance. Hyponatremia is a common electrolyte abnormality caused by an actual sodium deficiency or extracellular compartment fluid excess. Clinical symptoms are related with acuity and speed with which this abnormality is established. The symptoms are mainly neurological and neuromuscular disorders (headache, confusion, stupor, seizures, coma) due to brain cells edema. Hyponatremia due to sodium deficiency is caused by sodium loss from kidney (nephritis, diuretics, mineralocorticoid deficiency) and / or extrarenal (vomiting, diarrhea, burns). Hyponatremia due to water excess seems to be the most common and it is attributable to cirrhosis, nephrotic syndrome, heart failure, infusion 5% glucose solutions and drugs that stimulate ADH secretion. It was recently highlighted the role of inflammation and IL-6 in the non-osmotic ADH release. Hyponatremia is considered also marker of phlogosis. Acute (<48 h) and severe (<125 mEq/ L) hyponatremia is a medical emergency that requires prompt correction. Patients with chronic hyponatremia have a high risk of osmotic demyelination syndrome if rapid correction of the plasmatic sodium occurs. In combination with conventional therapy, a new class of drugs, vasopressin receptors antagonists (AVP-R antagonists) would be able to increase the excretion of electrolyte-free water and the serum sodium concentration.