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Hyponatraemia is the most common electrolyte disturbance observed in hospital inpatients. We report a 90-year-old woman admitted generally unwell following a fall with marked confusion. Examination revealed a tender suprapubic region, and investigations observed elevated inflammatory markers and bacteriuria. Admission investigations demonstrated a serum sodium of 110 mmol/L with associated serum osmolality 236 mmol/kg and urine osmolality 346 mmol/kg. She was treated for hyponatraemia secondary to syndrome of inappropriate antidiuretic hormone (SIADH) and urosepsis. However, her serum sodium failed to normalise despite fluid restriction, necessitating treatment with demeclocycline and hypertonic saline. Despite slow reversal of hyponatraemia over 1 month, the patient developed generalised seizures with pontine and thalamic changes on MRI consistent with osmotic demyelination syndrome (ODS). This case highlights the risk of ODS, a rare but devastating consequence of hyponatraemia treatment, despite cautious sodium correction.

Background The hyperosmolar hyperglycemic state (HHS), an acute complication of diabetes mellitus with plasma hyperosmolarity, promotes the secretion of anti-diuretic hormone (ADH) and reduces the storage of ADH. Magnetic resonance T1-weighted imaging reflects ADH storage in the posterior pituitary lobe, which disappears when the storage is depleted. Whether the HHS induces ADH depletion leading to clinical manifestations has been unclear. Case report A 55-year-old Japanese woman was admitted to our center because of mental disturbance and hypotension. She had received lithium carbonate for bipolar disorder and presented with polydipsia and polyuria from 15 years of age. On admission, she had mental disturbance (Glasgow Coma Scale, E4V1M1), hypotension (systolic blood pressure, 50 mmHg), and tachycardia (pulse rate, 123/min). Plasma glucose was 697 mg/dL osmolality was 476 mOsm/kg•H2O, and bicarbonate was 23.7 mmol/L. The diagnoses of HHS and hypovolemic shock were made. During treatment with fluid replacement and insulin therapy, the urine volume continued to be approximately 3 to 4 L/day, and an endocrine examination revealed ADH insufficiency and nephrogenic diabetes insipidus. Desmopressin 10 μg/day and trichlormethiazide 2 mg/day were necessary and administered, and the endogenous ADH secretion improved gradually. The signal intensity of the pituitary posterior lobe, initially decreased on magnetic resonance T1 images, was also improved. Conclusion This patient had ADH insufficiency associated with ADH depletion due to hyperosmolarity and nephrogenic diabetes insipidus. Clinicians should be aware of the risk of the development of critical HHS and relative ADH insufficiency in patients being treated with lithium carbonate.

OBJECTIVE To describe a case of inappropriate antidiuretic hormone (ADH) secretion in a dog secondary to trauma. CASE SUMMARY A 14-year-old neutered female mixed breed dog presented for evaluation of bite wounds. The dog sustained multiple puncture wounds to the cervical area, stifle, and elbow. Treatment was initiated with isotonic crystalloid fluids, analgesia, broad-spectrum antimicrobials, and gastroprotectants. The dog developed hyponatremia with concurrent serum hypoosmolality and inappropriate urine hyperosmolality and urine sodium secretion, leading to a diagnosis of the syndrome of inappropriate ADH secretion. The hyponatremia improved, and the dog improved clinically and was discharged 3 days after admission. NEW OR UNIQUE INFORMATION PROVIDED This is the first case description of the syndrome of inappropriate ADH secretion in a dog suffering from trauma. Inappropriate ADH secretion is largely under-recognized in veterinary patients. Increased awareness of this syndrome can lead to initiation of appropriate treatment and improved outcomes.

Tuberculous meningitis (TBM) is a common infection of the central nervous system. TBM with hyponatremia is very common. If hyponatremia is not treated properly, it might affect the outcome of TBM patients. We included 226 patients diagnosed with TBM who were admitted from August 2010 to August 2015 and retrospectively analyzed the clinical data of patients with and without hyponatremia. In total, 45.6% (103/226) patients had hyponatremia and 54.4% (123/226) patients did not have hyponatremia. Serum sodium and severity of TBM were independent prediction factors of poor outcomes in TBM. The prognosis of patients with hyponatremia was worse than that of patients without hyponatremia. The mortality was 3.9% (4/103) in the hyponatremia group, while 0% (0/123) in the non-hyponatremia group. The degree of hyponatremia was related to imaging, cerebrospinal fluid (CSF) cell count and protein, severity of TBM, time to correct hyponatremia, and prognosis. We analyzed the causes of hyponatremia and found syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was the most common cause (77.7%, 80/103), followed by cerebral salt wasting (CSW) (17.5%, 18/103). Comparing SIADH and CSW, there was a significant difference in mean blood pressure, albumin, and hematocrit, and no significant difference in demographic characteristics, imaging, CSF cell count and protein, severity, occurrence and correction time of hyponatremia, or prognosis. TBM with hyponatremia was dominated by moderate hyponatremia, which often manifested as SIADH. The more severe hyponatremia was, the longer the correction time of hyponatremia, which will affect the prognosis of TBM patients.

Hyponatremia, especially if acute and severe, can be a life-threatening condition. Several conditions can trigger hyponatremia. In this review, we will discuss two conditions that can determine euvolemic hyponatremia: the cerebral/renal salt wasting (CRSW) syndrome and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), including the two subtypes: reset osmostat (RO) and nephrogenic syndrome of inappropriate antidiuresis (NSIAD) and their differential diagnoses. Despite the passage of over 70 years since its first description, to date, the true etiopathogenesis of CRSW syndrome, a rare cause of hypovolemic/euvolemic hyponatremia, is almost unknown. SIADH, including RO and NSIAD, is sometimes difficult to differentiate from CRSW syndrome; in its differential diagnosis, the clinical approach based on the evaluation of the extracellular volume (ECV) was proven insufficient. We therefore suggest a simple diagnostic algorithm based on the assessment of the degree of hyponatremia, urinary osmolality, and the assessment of the fraction of urate excretion (FEUa) in conditions of hyponatremia and after serum sodium correction, to be applied in children over 1 year of life.

The consumption of new selective serotonin reuptake inhibitors (SSRIs) is raising dramatically especially in European countries. It contributes to occurrence of clinically important drug side effects. One of which can be hyponatremia. We present two case reports of 85-year-old and 84-year-old women who developed hyponatremia after escitalopram administration. We hypothesize that in both cases hyponatremia was connected with antidepressants administration. However, due to multiple comorbidities and polypharmacy it is often impossible to establish the exact mechanism of hyponatremia. Moreover, it is crucial to distinguish subtypes of drug-induced syndrome of inappropriate antidiuretic hormone hypersecretion (SIADH), such as SSRI-induced SIADH, reset osmostat SIADH, thiazide-associated hyponatremia, thiazide-induced hyponatremia, mineralocorticoid responsive hyponatremia of older adults, in order to properly diagnose and treat geriatric patients. Administration of antidepressants or thiazides should be followed by a regular monitoring of serum sodium level.

The endocrine paraneoplastic manifestations of cancer are well described and result from ectopic hormone production by non-endocrine organs or direct hormone secretion from endocrine malignancies. However, an emergent and more common issue is that of endocrine dysfunction associated with systemic anti-cancer therapies. These often present with vague symptoms but can be life-threatening and therefore awareness of these is essential. Here, we review the three most common paraneoplastic manifestations of cancer (hypercalceamia, syndrome of inappropriate antidiuretic hormone, Cushing's syndrome) and provide an overview of the endocrine complications of systemic anti-cancer therapies.

Tubulopathies are a group of heterogeneous diseases that are manifested in the malfunction of the renal tubules. This review addresses tubulopathies associated with polyuria syndrome, namely renal glucosuria syndrome, nephrogenic diabetes insipidus and pseudohyperaldosteronism. Types of renal glucosuria are described, namely: type A, type B and the most severe type 0. Type A is characterized by a low filtration threshold and low glucose reabsorption. The type of inheritance is autosomal recessive. Type B, autosomal dominant, is characterized by uneven activity of glucose transport, in which its reabsorption is reduced only in some nephrons. That is, normal reabsorption of glucose is maintained, but the filtration threshold of the latter is reduced. Type 0 with a severe course is characterized by complete inability of epithelial cells of the proximal tubules to reabsorb glucose. Nephrogenic diabetes insipidus is a rare inherited disease caused by impaired response of the renal tubules to antidiuretic hormone (ADH). Depending on the degree of inability to concentrate urine, there are complete and partial forms. It is divided into nephrogenic diabetes insipidus type I (X-linked recessive); nephrogenic diabetes insipidus type II (autosomal recessive and autosomal dominant) and nephrogenic diabetes insipidus syndrome with dementia and intracerebral calcifications (type of inheritance remains unknown). Children with autosomal recessive type of inheritance suffer from the more severe disease course. Pseudohypoaldosteronism is characterized by a special condition of the renal tubules which is due to insufficient sensitivity of the tubular epithelium to aldosterone, which in turn leads to hyperaldosteronism, the development of hyponatremia, metabolic acidosis with hyperkalemia, polydipsia and polyuria, decreased sodium reabsorption and retardation of the child's physical development. The classification includes three syndromes of pseudohypoaldosteronism, namely: type I (PHA1), which is divided into PHA1A (autosomal dominant, renal), PHA1B (autosomal recessive, systemic); type II (PHA2; Gordon’s syndrome), type III (secondary), which develops as a result of renal pathology.

We present a case of severe hyponatraemia due to syndrome of inappropriate antidiuretic hormone (SIADH) in a patient with respiratory syncytial virus (RSV) infection. A retrospective analysis of all patients admitted to our hospital with RSV in the preceding 3-year period revealed hyponatraemia in 41 (28%) cases, of which 13 (8.9%) were moderate or severe. SIADH was explored and confirmed in five (3.4%) patients, raising this as an important, previously unrecognised, complication of RSV infection in adults. Physician awareness of SIADH as a potential complication of RSV will facilitate early diagnosis and treatment of this potentially fatal disorder.

BACKGROUND Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is relatively common in several cancers, such as small cell lung cancer. However, nedaplatin-induced SIADH is rare. We describe a case of SIADH mediated by nedaplatin. CASE SUMMARY A 54-year-old female with nasopharyngeal carcinoma was treated with nedaplatin and developed severe hyponatremia due to SIADH. The side effects were successfully treated by fluid restriction and sodium supplementation. CONCLUSION This case report highlights the importance of cautiously treating life-threatening hyponatremia in patients treated with nedaplatin.

Purpose. The dynamic state of epinephrine (Ep) in the plasma of patients with out-of-hospital cardiac arrest (OHCA) remains unclear. The purpose of this study was to evaluate the relationship between the plasma levels of catecholamines (such as epinephrine (Ep), norepinephrine (Nep), and dopamine) and vasopressin (antidiuretic hormone (ADH)) and the acquisition of return of spontaneous circulation (ROSC) in OHCA patients. Methods. This was a prospective, observational clinical study. Patients with OHCA transferred to our hospital between July 2014 and July 2017 were enrolled. The levels of catecholamines and ADH in the plasma were measured using blood samples immediately obtained on arrival at our hospital and before the administration of Ep. Patients in whom Ep was already administered prior to obtaining blood samples were excluded. Patients were divided into two groups: with and without ROSC, that is, ROSC (+) and ROSC (−) groups, respectively. The plasma levels of these agents and the conditions of resuscitation were compared between the two groups. Results. A total of 96 patients with OHCA were analyzed. The ROSC (+) and ROSC (−) groups included 34 and 62 patients, respectively. There were no significant differences observed between the two groups in age, cause of cardiopulmonary arrest, and prehospital resuscitation time. The plasma levels of Ep and Nep were significantly lower in the ROSC (+) group than in the ROSC (−) group. However, there were no significant differences in the plasma levels of dopamine and ADH between the two groups. Conclusion. Increased levels of Ep in the plasma may not be associated with the acquisition of ROSC in patients with OHCA.

Syndrome of inappropriate antidiuretic hormone (SIADH) secretion is a recognisable complication of acute porphyria. We report a nine-year-old female patient with hereditary tyrosinaemia type 1 and poor adherence to nitisinone therapy who presented with acute abdominal pain, vomiting and lethargy at Sultan Qaboos University Hospital, Muscat, Oman in 2016. She subsequently developed generalised tonic-clonic seizures attributable to severe hyponatremia that met the diagnostic criteria of SIADH. The acute porphyria screen also appeared positive. The patient responded well to fluid restriction and was discharged home without immediate neurological sequelae. Although acute porphyria is also a recognised complication of uncontrolled tyrosinaemia type 1, to the best of the authors’ knowledge, no patient with tyrosinaemia type 1 has been reported to present with SIADH. Keywords: Tyrosinemia Type 1; Hyponatremia; Inappropriate ADH Syndrome; Case Report; Oman.

Hyponatremia is the most common disorder of water and electrolyte balance encountered in clinical practice. Conditions associated with hyponatremia require hospitalization in 15–20% of cases. Hyponatremia is a predictor of poor outcome in a wide range of diseases and therefore requires an interdisciplinary approach. This problem leads to an increase in complications and the length of hospital stay and mortality. The review focuses on the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), which accounts for approximately one third of all cases of hyponatremia and is more common in endocrinology than other fluid and electrolyte disorders along with central diabetes insipidus. The article presents modern approaches to the treatment of SIADH based on international clinical guidelines.

We report a 72-year-old woman with Miller-Fisher syndrome (MFS) with syndrome of inappropriate secretion of antidiuretic hormone (SIADH). She developed diplopia and unsteady gait a week after an upper respiratory infection. Neurologic examination revealed ophthalmoplegia, ataxia, symmetrical weakness, numbness, and areflexia. She underwent intravenous immunoglobulin therapy. Her serum sodium concentration decreased to 119 mEq/L on day 12. She had low plasma osmolarity (254 mosm/kg), high urine osmolarity (457 mosm/kg), and high urine sodium level (73 mEq/L), while the blood level of antidiuretic hormone was normal. Anti-GD1b immunoglobulin G (IgG), -GQ1b IgG, -GT1a IgG, and -Gal-C IgM antibodies were positive. We diagnosed her with MFS overlapping with SIADH. Four weeks after onset, her symptoms recovered. The elevation of anti-GD1b, -GQ1b, and -GT1a antibodies that recognize disialosyl residue may be pathologically related to SIADH.

The use of tolvaptan to treat both euvolemic and hypervolemic hyponatremia has rapidly increased in recent years. However, data on its effects on children, especially newborns and infants, are limited. Here, we present a newborn who developed syndrome of inappropriate secretion of antidiuretic hormone following an intracranial hematoma drainage operation who was unresponsive to conventional treatments. The infant was successfully treated with tolvaptan, a competitive inhibitor of the vasopressin V2 receptor.

Background Coronavirus Disease-2019 (COVID-19) has been declared a global pandemic since March 11th, 2020. Despite emerging reports and literature covering a broad spectrum of COVID-19 clinical manifestations, facets of COVID-19 have not been fully elucidated. To the authors’ concern, sinus bradycardia as a manifestation of COVID-19-induced syndrome of inappropriate antidiuretic hormone (SIADH) has never been reported before. Case presentation In this paper, we report a case of a 59-year-old male patient with confirmed COVID-19 initially presented with presyncope. Further investigations reveal sinus bradycardia related to COVID-19-induced SIADH. This case highlights the possibility of immuno-neuroendocrino-cardiovascular crosstalk resulting in an atypical manifestation of COVID-19: near syncope due to sinus bradycardia. Conclusions Another possible cause of sinus bradycardia in COVID-19 is electrolyte imbalance due to COVID-19-related SIADH.

Current study is a case report of a 5-year-old patient with T-cell acute lymphoblastic leukemia (ALL) and multiple urolithiasis. Complex factors, including glucocorticoid-induced hypercalciuria, fluid restriction for the syndrome of inappropriate secretion of antidiuretic hormone, and long-term bed rest, predispose children with ALL to develop urolithiasis. To prevent urinary urolithiasis formation, urinary calcium excretion should be monitored during chemotherapy and when administering glucocorticoids.

Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a disease that leads to dilute hyponatremia through excessive secretion of antidiuretic hormone. SIADH has various causes, including ectopic ADH-producing tumors, drug properties, and can be idiopathic. But there have been very few reports of cases in which SIADH has developed after surgery for malignant tumors. In addition, few cases have been reported where this disease has developed after surgery for pancreatic cancer, because the symptoms of hyponatremia are non-specific. These symptoms are particularly gastrointestinal symptoms; therefore, it is difficult to differentiate them, even if SIADH has developed after gastrointestinal surgery. The patient in our case was an 80-year-old woman. She had persistent epigastralgia and left back pain. Imaging studies revealed a tumor in the head of the pancreas, which was diagnosed as pancreatic head cancer. We performed subtotal stomach-preserving pancreatoduodenectomy. After the operation, she complained of appetite loss and general fatigue. Her serum sodium levels decreased to 109 mEq/L on postoperative day 11. She was diagnosed with SIADH using the SIADH diagnostic criteria listed by the Japanese Ministry of Health, Labor and Welfare. We treated the patient with sodium supplementation for hyponatremia, and her symptoms ameliorated. After the event, she did not relapse with hyponatremia. This case is significant in that we performed differential diagnosis after major gastrointestinal surgery for pancreatic cancer and diagnosed SIADH at an early stage.

Background The most vexing problem in hyponatremic conditions is to differentiate the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from cerebral/renal salt wasting (C-RSW). Both have identical clinical parameters but diametrically opposite therapeutic goals of water- restricting water-logged patients with SIADH or administering salt and water to dehydrated patients with C-RSW. While C-RSW is considered a rare condition, the report of a high prevalence of C-RSW in the general hospital wards creates an urgency to differentiate one syndrome from the other on first encounter. We decided to identify the natriuretic factor (NF) we previously demonstrated in plasma of neurosurgical and Alzheimer diseases (AD) who had findings consistent with C-RSW. Methods We performed the same rat renal clearance studies to determine natriuretic activity (NA) in serum from a patient with a subarachnoid hemorrhage (SAH) and another with AD and demonstrated NA in their sera. The sera were subjected to proteomic and SWATH (Sequential Windowed Acquisition of All) analyses which identified increased levels of haptoglobin related protein (Hpr) without signal peptide (Hpr-WSP). Results Recombinant Hpr with His tag at the N terminus had no NA. Hpr-WSP had a robust NA in a dose-dependent manner when injected into rats. Serum after recovery from C-RSW in the SAH patient had no NA. Conclusions Hpr-WSP may be the NF in C-RSW which should be developed as a biomarker to differentiate C-RSW from SIADH on first encounter, introduces a new syndrome of C-RSW in AD and can serve as a proximal diuretic to treat congestive heart failure.

Low molecular weight heparin-induced hyperkalemia is not an uncommon side effect. The development of hyponatremia is well described although it is less common. We report a 72-year-old woman with lumbar metastases who developed hyponatremia and hyperkalemia on the tenth day of hospitalization. Hyponatremia, with limited criteria for syndrome of inappropriate secretion of antidiuretic hormone, did not resolve with vigorous volume restriction. Hyperkalemia without an acid-base disorder or baseline renal failure, did not resolve after losartan was stopped. Enoxaparin-induced hypoaldosteronism was proposed and the drug was discontinued. After four days’ persistence of the electrolyte disturbance, dexamethasone was changed to Hydrocortisone, and parameters normalized in 24 hours. The patient remained well until discharge and during outpatient control.

Cerebral salt wasting (CSW) is an uncommon cause of hyponatremia characterized by extracellular volume depletion, high urine sodium concentration and osmolality, and low serum uric acid concentration in association with central nervous system (CNS) disease. Distinguishing CSW from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), a much more common form of hyponatremia in this setting, can be challenging because both present with identical laboratory features. However, treatment of CSW and SIADH differs, making a correct diagnosis important. Here we present a case of CSW in a 75-year-old man in whom severe hyponatremia and volume depletion were discovered in the setting of traumatic head injury and Dandy-Walker malformation of the brain, a rare congenital brain malformation. Treatment with intravenous normal saline and later oral salt supplementation and fludrocortisone was successful.

Syndrome of inappropriate antidiuretic hormone (SIADH) is a disorder of fluid and sodium balance characterized by hypotonic hyponatremia, low plasma osmolality, and increased urine osmolality caused by excessive release of antidiuretic hormone (ADH). Malignancy is one of the most common causes of SIADH, but SIADH in esophageal carcinoma is very rarely reported. In this case report, a 74-year-old male patient of moderate differentiation of squamous cell esophageal carcinoma had a recurrent electrolyte balance disorder despite repeated corrections. The patient experienced improvement after fluid restriction and drug administration.

Introduction and hypothesis Nocturia, defined as the act of waking to pass urine during sleeping, is a common problem in older women and is associated with significant morbidity and impairments in health-related quality of life. The aim of this review was to synthesize the current evidence regarding the incidence, impact, pathophysiology, and specific diagnostic approach of nocturia in the postmenopausal population. Methods We searched PubMed and Web of Science databases to identify relevant studies published through June 2020. Reference lists of the reviews obtained were screened for other articles deemed pertinent by the authors. Results Genitourinary symptoms attributed to the menopause have been reported to occur in nearly 90% of postmenopausal women, and nocturia is one of the most common. The relative deficiency in endogenous estrogen production after the menopause is thought to exacerbate all major pathophysiological mechanisms that may underlie nocturia, including reduced bladder capacity, nocturnal polyuria, global polyuria, and sleep disorders. Diminished estrogen may induce anatomical and physiological bladder changes, contributing to a reduction in functional bladder capacity. Excess nocturnal urine production can also be provoked by estrogen depletion, either via free water-predominant diuresis by an impaired secretion of antidiuretic hormone, or a salt-predominant diuresis owing to diminished activation of the renin-angiotensin-aldosterone axis. Additionally, a relationship between the transition to menopause and impaired sleep has been described, mediated by increased incidence in vasomotor symptoms and obstructive sleep apnea signs during the menopause. Conclusion Further research is necessary to better characterize and manage nocturia in postmenopausal women.

Objective: To review and report the results in pure endoscopic endonasal trans-sphenoidal surgery done at our unit for pituitary adenomas (PAs) in last 8 years. Material and Methods: We reviewed 403 consecutive patients who underwent pure endoscopic endonasal trans-sphenoidal surgery for newly diagnosed pituitary adenomas between August 2012 and July 2020 at our neurosurgical unit. Endocrinological, demographic features and outcomes, their complications, and duration of stay in hospital were assessed in these patients who were operated in our neurosurgical Unit. The Mean Follow-up on average was 3.5 months. Results: 403 consecutive cases were reviewed. Majority of cases were in the 4th decade of life at presentation. 227 (56%) were non-functioning pituitary tumors and 176 (44%) were hormone secreting pituitary adenomas. Thirty-one (7.7%) complications were observed in 28 post-operative patients. The most frequently observed complication was diabetes insipidus (temporary in 19 (5%) and permanent in 3 (0.7%) cases), cerebrospinal fluids leaks (5 cases) (5.7%), Syndrome of inappropriate antidiuretic hormone (1 case) (0.2%), internal carotid injury (1 case) (0.2%), Empty Sella syndrome (1) (0.2%) and post-operative cardiac complication (1 case) (0.2%). The Follow-up on average was 3.5 months. Conclusions: The pure endoscopic endonasal trans-sphenoidal surgery of pituitary adenomas provides acceptable and reasonable results representing a safe alternative procedure to the traditional Trans-sphenoidal microscopic approach.

Recently, chronic hyponatremia, even mild, has shown to be associated with poor quality of life and high mortality. The mechanism by which hyponatremia contributes to those symptoms, however, remains to be elucidated. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a primary cause of hyponatremia. Appropriate animal models are crucial for investigating the pathophysiology of SIADH. A rat model of SIADH has been generally used and mouse models have been rarely used. In this study, we developed a mouse model of chronic SIADH in which stable and sustained hyponatremia occurred after 3-week continuous infusion of the vasopressin V2 receptor agonist 1-desamino-8-D-arginine vasopressin (dDAVP) and liquid diet feeding to produce chronic water loading. Weight gain in chronic SIADH mice at week 2 and 3 after starting dDAVP injection was similar to that of control mice, suggesting that the animals adapted to chronic hyponatremia and grew up normally. AQP2 expression in the kidney, which reflects the renal action of vasopressin, was decreased in dDAVP-infused water-loaded mice as compared with control mice that received the same dDAVP infusion but were fed pelleted chow. These results suggest that "vasopressin escape" occurred, which is an important process for limiting potentially fatal severe hyponatremia. Behavioral analyses using the contextual and cued fear conditioning test and T-maze test demonstrated cognitive impairment, especially working memory impairment, in chronic SIADH mice, which was partially restored after correcting hyponatremia. Our results suggest that vasopressin escape occurred in chronic SIADH mice and that chronic hyponatremia contributed to their memory impairment.

Purpose The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a well-known complication of transsphenoidal pituitary surgery, related to inappropriate secretion of arginine vasopressin (AVP). Its diagnosis is based on hyponatremia, with a peak of occurrence around day 7 after surgery and, to date, no early marker has been reported. In particular, copeptin levels are not predictive of hyponatremia in this case. Oxytocin (OXT) is secreted into the peripheral blood by axon terminals adjacent to those of AVP neurons in the posterior pituitary. Besides its role in childbirth and lactation, recent evidences suggested a role for OXT in sodium balance. The contribution of this hormone in the dysnatremias observed after pituitary surgery has however never been investigated. Methods We analyzed the urinary output of OXT in patients subjected to transsphenoidal pituitary surgery. Results While OXT excretion remained stable in patients who presented a normonatremic postoperative course, patients who were later diagnosed with SIADH-related hyponatremia presented with a significantly increased urinary secretion of OXT 4 days after surgery. Conclusion Taken together, these results show for the first time that urinary OXT output remains normally stable after transsphenoidal pituitary surgery. OXT excretion however becomes abnormally high on or around 4 days after surgery in patients later developing hyponatremia, suggesting that this abnormal dynamics of OXT secretion might serve as an early marker for transsphenoidal surgery-related hyponatremia attributed to SIADH.

Introduction Pulmonary tuberculosis (PTB) is one of the rare pulmonary infections causing hyponatremia (serum sodium ˂135 mmol/L) and severe hyponatremia (serum sodium ˂125 mmol/L). Although the major cause of hyponatremia in TB patients is syndrome of inappropriate antidiuretic hormone (SIADH) secretion, cerebral salt wasting syndrome (CSWS) can occur and requires evidence of inappropriate urinary salt losses and reduced arterial blood volume. Adrenal insufficiency (AI) is rare in TB with scanty literature describing it. The two reported cases highlight three possible causes of severe symptomatic hyponatremia in TB pleural effusion and disseminated TB, their treatment modalities, and the need to increase the index of suspicion to diagnose TB hyponatremia in children. Case Report Case 1: a 10-year-old girl with TB pleural effusion who developed recurrent hyponatremia in the first few weeks of anti-TB treatment which was responsive to sodium correction. Case 2: an 8-year-old girl presenting to our facility with presumptive TB. She deteriorated over several months and progressed to disseminated TB with AI. Discussion Early diagnosis and prompt and correct treatment of TB hyponatremia cannot be overemphasized, as AI, SIADH secretion, and CSWS, each require different therapeutic regimens, most especially AI on its own poses a huge clinical challenge. Conclusion A high index of suspicion, with intensified case finding at all levels of care, is necessary to identify and manage children with TB hyponatremia because early diagnosis and prompt treatment is lifesaving.

IntroductionDiabetes insipidus (DI) is characterized by the excretion of large volumes of hypotonic urine and thirst due to an impaired ability to concentrate urine, leading to uncontrolled diuresis, which may cause life-threatening dehydration and electrolyte imbalances. Central DI is caused by the deficient secretion of the posterior pituitary antidiuretic hormone arginine vasopressin (AVP). Desmopressin (Deamino-8-D-AVP, the synthetic analogue of AVP, Minirinmelt®) is generally used to treat central DI. Desmopressin orally disintegrating tablets are recently administered to male patients with nocturia. We herein attempted to select male patients with an elevated nocturnal urinary frequency possibly due to a shortage of AVP. These patients may be good candidates for low-dose oral desmopressin administration.Patients and methodsSerum and spot urine osmolality, electrolytes, serum creatinine, casual blood glucose, plasma brain natriuretic polypeptide (BNP), and plasma AVP were measured at the same time in 97 elderly male patients with urinary symptoms under free water drinking. The International Prostate Symptom Score, Overactive Bladder Symptom Score, and frequency-volume charts at least twice were also evaluated.ResultsA binary plot of plasma AVP and serum osmolality indicated a region at which patients had relatively lower AVP considering higher serum osmolality. It was tentatively named the Desmopressin region. Twenty out of 97 (20.6 %) patients were in the Desmopressin region.No significant differences were observed in the frequency of administered urinary drugs or existing co-morbidities between patients in the Desmopressin and non-Desmopressin regions. Daily urine output did not exceed 3 L in any patient. Plasma AVP was lower, while serum osmolality and serum sodium were higher in patients in the Desmopressin region than in those in non-Desmopressin region. Furthermore, urine osmolality was slightly lower in patients in the Desmopressin region. No significant differences were observed in urine volume, urinary frequency, or urination questionnaire scores between both groups.ConclusionAVP-shortage patients may be selected for treatment with oral desmopressin based on measurements of serum osmolality and plasma AVP. After the exclusion of patients with marked hyperglycemia, decreased cardiac, or renal function, low-dose oral desmopressin may be administered to patients with an increased urine output, nocturia, elevated plasma osmolality, and relatively low plasma AVP.

Background Hypochloremia associated with congestive heart failure (CHF) in dogs is likely multifactorial. Loop diuretics cause 1:2 sodium [Na+]:chloride [Cl−] loss, whereas water retention causes a 1:1 [Na+]:[Cl−] dilution. Mathematical [Cl−] correction separates these effects on [Cl−]. Hypothesis We hypothesized that corrected [Cl−] (c[Cl−]) would not differ from measured [Cl−] (m[Cl−]) in dogs with controlled CHF because of loop diuretics, and dogs with refractory CHF would have higher c[Cl−] than m[Cl−], indicating relative water excess. Animals Seventy‐one client‐owned dogs with acquired heart disease, without CHF (NO‐CHF), 76 with Stage C CHF and 24 with Stage D CHF. Methods Clinicopathological data from a previous study were retrospectively analyzed. Corrected [Cl−], m[Cl−], and differences were compared among NO‐CHF, Stage C CHF, and Stage D CHF, using the formula: c[Cl−] = (mid‐reference range [Na+]/measured [Na+]) × m[Cl−]. Results Corrected [Cl−] and m[Cl−] were lower in Stage D vs Stage C and NO‐CHF (all P 2 mmol/L. Conclusions and Clinical Importance Serum [Cl−] increased after mathematical correction in Stage D CHF dogs but not in Stage C and NO‐CHF dogs. Although c[Cl−] was higher than m[Cl−] in Stage D dogs supportive of relative water excess, hypochloremia persisted, consistent with concurrent loop diuretic effects on electrolytes. Future study correlating c[Cl−] to antidiuretic hormone concentrations is warranted.

The study of eye hydrodynamics following five-day “dry” immersion (DI) was aimed at evaluating the influence of compensatory body hypohydration on the intraocular hydrodynamic balance. For the first time the data of electronic eye tonography before and after modeled microgravity were compared. The study involved ten male volunteers 24 to 40 years of age without ophthalmologic pathologies. Electronic eye tonography results and hypohydration dynamics were assessed by fluid balance. Electronic tonography was performed before DI and on post-DI days 1 and 7 to measure the true intraocular pressure and to calculate the intraocular fluid production rate (F), coefficient of aqueous humor outflow ease, Bekker coefficient, and trophic coefficient (TC). On post-DI day 1, F reduction was observed in eight volunteers (60% of cases, 12 eyes). Level of the F reduction varied from 40% of the baseline value (5 eyes) to abnormally low 54% (7 eyes) underlying trophic changes. TC went down in 60% of cases (12 eyes); in 50% of cases (6 eyes) TC reduction was clinically significant. By the seventh day after DI, intraocular hydrodynamics was comparable with the baseline. It is hypothesized that the reflectory hypohydration during DI (the Gauer–Henry reflex) is responsible for changes in the intraocular hydrodynamics; the depth of these changes is determined by the degree of compensatory hypothalamic influence upon the antidiuretic hormone-angiotensin II system.

Objectives Clinical and laboratory data of reset osmostat (RO) and cerebral/renal salt wasting (C/RSW) mimic syndrome of inappropriate antidiuretic hormone (SIADH) and can pose diagnostic challenges because of significant overlapping between clinical and laboratory findings. Failure to correctly diagnose hyponatremia may result in increased mortality risk, longer hospital stay, and is cost-effective. We aim to illustrate clinical and laboratory similarities and difference among patients with hyponatremic disorders and discuss the diagnostic value of factional uprate excretion (FEurate) to differentiate SIADH from RO and C/RSW. Case presentations We report the use of FEurate in the evaluation of three patients with hyponatremia and elevated urine osmolality in the absence of edema or clinical evidence of dehydration to differentiate SIADH from RO and C/RSW. Conclusions Measurement of FEurate may offset in part the diagnostic confusion imparted by the diagnoses of SIADH, RO, and C/RSW.

MR spectroscopy in a patient with hyponatremic encephalopathy due to the syndrome of inappropriate secretion of antidiuretic hormone revealed decreased N-acetyl-aspartate, creatine plus phosphocreatine, choline-containing compounds, and myo-inositol, with normal glutamate and increased glutamine, which normalized after Na normalization. The decreased concentrations of creatine plus phosphocreatine, choline-containing compounds and myo-inositol are explained by their release as osmolytes from brain cells to adapt to hypo-osmolality induced cerebral edema. Increased glutamine, which not only acts as an osmolyte but also protects neurons under excitotoxic conditions, may suggest that a disrupted glutamate-glutamine cycle may play an important role in the pathogenesis of hyponatremic encephalopathy.

BACKGROUND Several studies have demonstrated that non-osmotic antidiuretic hormone activity contributes to the development of hyponatremia in children with common febrile diseases. However the relationship between hyponatremia and body temperature has remained unclear. Therefore, we examined this relationship in children with common diseases. METHODS In this retrospective case study based on chart review, 1,973 children presenting with acute illnesses at Hirakata City Hospital between November 2008 and October 2009, and for whom blood test data were available, were enrolled. The median age of this cohort was 2.7 years and the mean serum sodium concentration was 136.4 mEq/L; 454 patients showed hyponatremia (

Introduction Central diabetes insipidus is a heterogeneous condition characterized by decreased release of antidiuretic hormone by the neurohypophysis resulting in a urine concentration deficit with variable degrees of polyuria. The most common causes include idiopathic diabetes insipidus, tumors or infiltrative diseases, neurosurgery and trauma. Temozolomide is an oral DNA-alkylating agent capable of crossing the blood-brain barrier and used as chemotherapy primarily to treat glioblastoma and other brain cancers. Cases Two men (aged 38 and 54 years) suddenly developed polyuria and polydispsia approximately four weeks after the initiation of temozolomide for a glioblastoma. Plasma and urine parameters demonstrated the presence of a urinary concentration defect. Management The clinical and laboratory abnormalities completely resolved with intranasal desmopressin therapy, allowing the continuation of temozolomide. The disorder did not relapse after cessation of temozolomide and desmopressin and relapsed in one patient after rechallenge with temozolomide. Discussion Our report highlights the importance of a quick recognition of this exceptional complication, in order to initiate promptly treatment with desmopressin and to maintain therapy with temozolomide.

Instruction Hyponatremia can be caused by various conditions such as Cerebral Salt Wasting Syndrome (CSWS), Inadequate Antidiuretic Hormone Secretion (SIADH), secondary adrenal dysfunction and thyroid dysfunction. However, each diagnosis has different treatment and inadequate treatment may increase mortality and morbidity, especially CSWS and SIADH. To the best of our knowledge, this case is considered rare clinical scenario and we would summarize some diagnostic criteria for these two diseases in this case report. Case presentation A 44-year-old Asian man was presented with cerebral salt wasting syndrome and elevated brain natriuretic peptide (BNP) after 2 weeks of a mild traumatic brain injury. Central nervous system examination revealed GCS 14 without neurological or neurosurgical deficit as well as cardiovascular history. CT scan showed right temporal hemorrhage #1.4 × 1.5 cm, scattered subarachnoid hemorrhages in the right hemisphere. The patient was treated in the direction of CSWS and symptoms of hyponatremia improved after 7 days. Re-examination after 3 months did not show any abnormal symptoms, sodium serum level returned to normal. Conclusion Hyponatremia caused by CSWS may occur in mild traumatic brain injury. Therefore, an accurate diagnosis and proper differentiation from SIADH is necessary to obtain an appropriate treatment with fluid and salt replacement. In this way, the patient morbidity and mortality can be reduced significantly.

Syndrome of inappropriate antidiuretic hormone release (SIADH) is a condition defined by the unsuppressed release of antidiuretic hormone (ADH) from the pituitary gland or nonpituitary sources or its continued action on vasopressin receptors. Of the many causes of SIADH, an important one includes tumours that secrete ADH. We describe a rare case of a patient with colonic adenocarcinoma presenting initially as SIADH. A 60-year-old man presented with confusion and vomiting. Over the previous month he had fatigue and loss of weight. Baseline investigations showed a low serum sodium level of 108mmol/l. He was euvolaemic on examination and fulfilled the criteria for SIADH. Further evaluation and imaging tests revealed that the patient had adenocarcinoma of the colon. It is remarkable that our patient did not present with any of the cardinal symptoms/signs suggestive of colorectal carcinoma including haematochezia, change in bowel habits or iron-deficiency anaemia. Initial therapy with hypertonic saline, fluid restriction and salt diet for management of SIADH was unsuccessful. Tolvaptan was added to the treatment regimen and the patient improved dramatically. Oncology consultation was initiated, and chemotherapy for the carcinoma was planned.

Hyponatremia is frequently seen in patients with ascites secondary to advanced cirrhosis and portal hypertension. Although not apparent in the early stages of cirrhosis, the progression of cirrhosis and portal hypertension leads to splanchnic vasodilation, and this leads to the activation of compensatory mechanisms such as renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system, and antidiuretic hormone (ADH) to ameliorate low circulatory volume. The net effect is the avid retention of sodium and water to compensate for the low effective circulatory volume, resulting in the development of ascites. These compensatory mechanisms lead to impairment of the kidneys to eliminate solute-free water in decompensated cirrhosis. Nonosmotic secretion of antidiuretic hormone (ADH), also known as arginine vasopressin, further worsens excess water retention and thereby hyponatremia. The management of hyponatremia in this setting is a challenge as conventional therapies for hyponatremia including fluid restriction and correction of hypokalemia are frequently inefficacious. In this review, we discuss the pathophysiology, complications, and various treatment modalities, including albumin infusion, selective vasopressin receptor antagonists, or hypertonic saline for patients with severe hyponatremia and those awaiting liver transplantation.