UNASSIGNED: Hyponatremia is a common electrolyte disorder. The severe hyponatremia has a mortality rate of 4%-40%. Psychiatric patients are likely to develop the condition because of polydipsia or the adverse effects of antipsychotics. We investigated the characteristics of patients with and without psychiatric diseases who developed severe hyponatremia.
UNASSIGNED: We retrospectively investigated cases admitted to our hospital (all departments) between October 2012 and November 2015 with a serum sodium concentration of ≤125 mmol/l on admission. We compared patient characteristics, etiology, and clinical course between psychiatric and nonpsychiatric patients.
UNASSIGNED: In total, 123 cases (62 female) were analyzed. Psychiatric disorders were present in 69 cases (56%), including schizophrenia (n = 19), anorexia (n = 16), mood disorders (n = 14), and organic mental disorders (n = 9). The mean patient age was 63 years. The mean serum sodium concentration on admission was 119 mmol/l, and the main causes of hyponatremia were polydipsia (20%), insufficient sodium intake (18%), and syndrome of inappropriate antidiuretic hormone secretion (16%). Compared with the nonpsychiatric group, the psychiatric group was significantly younger (55 vs. 74 years), was more likely to have polydipsia (30% vs. 6%), and had a lower in-hospital mortality (0% vs. 17%).
UNASSIGNED: Our study found differences in the clinical picture between psychiatric and nonpsychiatric patients with severe hyponatremia. Clinicians need to monitor serum sodium because the symptoms of hyponatremia can mimic those of psychiatric diseases.

OBJECTIVE: The syndrome of inappropriate antidiuresis (SIAD) can be treated with oral urea; however, compliance is impaired by its poor palatability.
OBJECTIVE: To investigate whether dietary proteins could increase plasma sodium levels through urea-induced osmotic diuresis.
METHODS: An open-label, proof-of-concept trial.
METHODS: University Hospital of Basel, Switzerland, between October 2021 and February 2023.
METHODS: Outpatients with chronic SIAD.
UNASSIGNED: Ninety grams of protein daily for 7 days in the form of protein powder, followed by 30 g of oral urea daily for 7 days after a wash-out period of ≥1 week.
METHODS: The increase in sodium levels from baseline to the end of the 7-day protein supplementation.
RESULTS: Seventeen patients were included. After 7 days of 90 g daily protein supplementation (n = 17), plasma sodium levels increased from 131 (129-133) to 133 (132-137), that is, by a median of 3 mmol L-1 (0-5) (P = .01). Plasma urea levels increased by 3 mmol L-1 (1.7-4.9) (P < .01), and urine urea to creatinine ratio increased by 21.2 mmol mmol-1 (6.2-29.1) (P < .01). After 7 days of 30 g oral urea (n = 10), plasma sodium levels increased from 132 (130-133) to 134 (131-136), that is, by a median of 2 mmol L-1 (1-3) (P = .06). Plasma urea levels increased by 5.8 mmol L-1 (2.7-9.2) (P < .01), and urine urea to creatinine ratio increased by 31.0 mmol mmol-1 (18.7-45.1) (P < .01).
CONCLUSIONS: Our findings suggest that protein powder increases plasma sodium levels in patients with chronic SIAD through protein-induced ureagenesis and osmotic diuresis. The effects are comparable with oral urea.

UNASSIGNED: Delayed postoperative hyponatremia (DPH) is common for sellar lesions. However, the true prevalence and associated factors of DPH after endoscopic endonasal surgery (EES) for Rathke\'s cleft cyst (RCC) have not been studied in a large patient cohort.
UNASSIGNED: A retrospective analysis was conducted over 6 years at our institution, and patients with RCC treated by EES were enrolled according to our inclusion criteria. Patient demographics, clinical characteristics, images, and surgical procedures were documented. Serum sodium was routinely measured before surgery, on postoperative day 1, and every 2 days thereafter until discharge. For patients with DPH, electrolyte, hematocrit, serum protein levels, and plasma and urinary osmolality were daily measured to explore potential etiology.
UNASSIGNED: Of the 149 eligible patients, 25 (16.8%) developed DPH, which was similar to other sellar lesions, except craniopharyngioma, in the same period in our institution. Significant risk factors suggested by univariate analysis were cyst location, requirement of postoperative hydrocortisone therapy, postoperative meningitis, intraoperative cerebrospinal fluid (CSF) leakage, and subtotal resection (STR) of the cyst wall (all p < 0.05). In addition, other supplementary 11 cases of suprasellar RCC with different surgical strategies (aggressive resection) and relevant factors were enrolled into multivariate analysis. Suprasellar location [odds ratio (OR) 8.387, 95% confidence interval (CI) 1.014-69.365, p = 0.049], requirement of postoperative hydrocortisone therapy (OR 4.208, 95%CI 1.246-14.209, p = 0.021), and intraoperative CSF leakage (OR 6.631, 95%CI 1.728-25.440, p = 0.006) were found to be the independent predictors of DPH.
UNASSIGNED: DPH is a common complication after EES for RCC. Suprasellar location, requirement of postoperative hydrocortisone therapy, and intraoperative CSF leakage are the most reliable risk factors. Cortisol deficiency and syndrome of inappropriate antidiuretic hormone (SIADH) are considered as the main etiologies of DPH in RCC. Conservative excision of the cyst wall may reduce DPH occurrence.

BACKGROUND: In patients receiving total parenteral nutrition (TPN), the frequency of hyponatraemia is high. However, the causes of hyponatraemia in TPN have not been elucidated, although diagnosis is required for appropriate therapy. The aim of this study is to describe the aetiology of hyponatraemia in non-critical hospitalised patients receiving TPN.
METHODS: Prospective multicentre study in 19 Spanish hospitals. Non-critically hyponatraemic patients receiving TPN and presenting hyponatraemia over a 9-month period were studied. Data collected included sex, age, previous comorbidities, and serum sodium levels (SNa) before and following TPN initiation. Parameters for study of hyponatraemia were also included: clinical volaemia, the presence of pain, nausea, gastrointestinal losses, diuretic use, oedema, renal function, plasma and urine osmolality, urinary electrolytes, cortisolaemia, and thyroid stimulating hormone.
RESULTS: 162 patients were included, 53.7% males, age 66.4 (SD13.8) years. Volume status was evaluated in 142 (88%): 21 (14.8%) were hypovolaemic, 96 (67.6%) euvolaemic and 25 (17.6%) hypervolaemic. In 111/142 patients the analytical assessment of hyponatraemia was completed. Hypovolaemic hyponatraemia was secondary to GI losses in 10/111 (9%), and to diuretics in 3/111 (2.7%). Euvolaemic hyponatraemia was due to Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH) in 47/111 (42.4%), and to physiological stimuli of Arginine Vasopressin (AVP) secretion in 28/111 (25.2%). Hypervolaemic hyponatraemia was induced by heart failure in 19/111 (17.1%), cirrhosis of the liver in 4/111 (3.6%).
CONCLUSIONS: SIADH was the most frequent cause of hyponatraemia in patients receiving TPN. The second most frequent cause was physiological stimuli of AVP secretion induced by pain/nausea.

BACKGROUND: In patients receiving total parenteral nutrition (TPN), the frequency of hyponatraemia is high. However, the causes of hyponatraemia in TPN have not been elucidated, although diagnosis is required for appropriate therapy. The aim of this study is to describe the aetiology of hyponatraemia in non-critical hospitalised patients receiving TPN.
METHODS: Prospective multicentre study in 19 Spanish hospitals. Non-critically hyponatraemic patients receiving TPN and presenting hyponatraemia over a 9-month period were studied. Data collected included sex, age, previous comorbidities, and serum sodium levels (SNa) before and following TPN initiation. Parameters for study of hyponatraemia were also included: clinical volaemia, the presence of pain, nausea, gastrointestinal losses, diuretic use, oedema, renal function, plasma and urine osmolality, urinary electrolytes, cortisolaemia, and thyroid stimulating hormone.
RESULTS: 162 patients were included, 53.7% males, age 66.4 (SD13.8) years. Volume status was evaluated in 142 (88%): 21 (14.8%) were hypovolaemic, 96 (67.6%) euvolaemic and 25 (17.6%) hypervolaemic. In 111/142 patients the analytical assessment of hyponatraemia was completed. Hypovolaemic hyponatraemia was secondary to GI losses in 10/111 (9%), and to diuretics in 3/111 (2.7%). Euvolaemic hyponatraemia was due to Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH) in 47/111 (42.4%), and to physiological stimuli of Arginine Vasopressin (AVP) secretion in 28/111 (25.2%). Hypervolaemic hyponatraemia was induced by heart failure in 19/111 (17.1%), cirrhosis of the liver in 4/111 (3.6%).
CONCLUSIONS: SIADH was the most frequent cause of hyponatraemia in patients receiving TPN. The second most frequent cause was physiological stimuli of AVP secretion induced by pain/nausea.

OBJECTIVE: To test the effectiveness of nurse-led dietary diabetes insipidus (DI) bundle on the severity of postoperative fluid imbalance in pituitary region tumours.
METHODS: Blinded randomized controlled trial.
METHODS: Patients aged 18-65 operated for sellar-suprasellar tumours in an Indian tertiary care centre were enrolled through total enumeration sampling and underwent randomization with allocation concealment during Sep 2018-Feb 2019. Pre-operative DI, postoperative ventilation, renal failure or decompensated diabetes mellitus were excluded. Patients in the intervention group received a nurse-led DI bundle (validated by three Delphi rounds) with four dietary components: intake of only water during thirst and avoidance of the following-added salt, high-protein foods and caffeinated drinks. Treating clinicians and the investigator assessing outcome were blinded about enrolment. Urine output, serum sodium, vasopressin requirement and hospital stay were assessed as primary outcomes. The outcome measures were monitored daily till the 6th postoperative day. Analyses were performed on \'intention-to-treat\' basis, irrespective of compliance. Independent t-test and Chi-square test were used.
RESULTS: Of the initial 63 patients, 50 fulfilling criteria were randomized to two groups and assessed over six days yielding 150 patient-days per group. There were no significant baseline differences between groups. The mean daily urine output was significantly lower in the DI bundle group than in control, both overall and among endonasal operated pituitary adenomas [3000.09(462.7) vs. 4095.71(896.4)ml & 2987.14(419.5) vs. 4064.73(1051)ml], with the greatest difference on the second postoperative day. Though hypernatraemia in controls became most prominent during days 2-3 and resolved in a week, it was significantly lower in the intervention group (12.7% vs. 30.7% overall, 11.4% vs. 29.4% endonasal adenomas). The need for vasopressin analogues and hospital stay were also significantly lower with DI bundle (p < 0.001).
CONCLUSIONS: This is probably the first ever report of dietary DI bundle among operated pituitary patients, which seem to flatten the DI trend with significant benefits in polyuria, hypernatraemia, vasopressin requirement and hospital stay.
BACKGROUND: CTRI/2018/07/015127 of ICMR.
CONCLUSIONS: The nurse-led dietary DI bundle has effectively reduced the severity of DI among operated pituitary patients with significant benefits in polyuria, hypernatraemia, vasopressin requirement and hospital stay. Its implementation is simple and easy to carry out, especially in resource-constrained institutions, where continuous monitoring and repeated serum sodium estimation are difficult.

Diuretics are often implicated in hyponatraemia. While thiazides constitute one of the most common causes of hyponatraemia, data on loop diuretics and potassium-sparing agents are limited and partly conflicting. The objective of this investigation was to study the association between use of different types of non-thiazide diuretics and hospitalization due to hyponatraemia.
This was a register-based case-control study on the adult Swedish population. By linking national registers, patients hospitalized with a principal diagnosis of hyponatraemia (n = 11,213) from 1 October 2005 through 31 December 2014 were compared with matched controls (n = 44,801). Multivariable logistic regression, adjusted for multiple confounders, was used to analyse the association between use of diuretics and hyponatraemia. In addition, newly initiated use (≤90 days) and ongoing use were examined separately.
Adjusted odds ratios (aORs) (95% CI) were 0.61 (0.57-0.66) for the use of furosemide, 1.69 (1.54-1.86) for the use of amiloride and 1.96 (1.78-2.18) for the use of spironolactone and hospitalization due to hyponatraemia. For newly initiated therapy, aORs ranged from 1.23 (1.04-1.47) for furosemide to 3.55 (2.75-4.61) for spironolactone. The aORs for ongoing use were 0.52 (0.47-0.57) for furosemide, 1.62 (1.47-1.79) for amiloride and 1.75 (1.56-1.98) for spironolactone.
Ongoing use of furosemide was inversely correlated with hospitalization due to hyponatraemia, suggesting a protective effect. Consequently, if treatment with furosemide precedes the development of hyponatraemia by some time, other causes of hyponatraemia should be sought. Spironolactone and amiloride may both contribute to hyponatraemia; this effect is most prominent early in treatment.

OBJECTIVE: Drug-induced hyponatremia is common, with medications from many drug-classes implicated. Lipid-lowering agents are among the most prescribed drugs. Limited evidence suggests an inverse association between statins and hyponatremia, while data on other lipid-lowering agents is absent. The objective of this investigation was to study the association between lipid-lowering drugs and hospitalization due to hyponatremia.
METHODS: This was a register-based case-control study of the general Swedish population. Those hospitalized with a main diagnosis of hyponatremia (n = 11,213) were compared with matched controls (n = 44,801). Multivariable logistic regression adjusting for co-medication, diseases, previous hospitalizations, and socioeconomic factors was used to explore the association between severe hyponatremia and the use of lipid-lowering drugs.
RESULTS: Unadjusted ORs (95% CI) for hospitalization due to hyponatremia were 1.28 (1.22-1.35) for statins, 1.09 (0.79-1.47) for ezetimibe, 1.38 (0.88-2.12) for fibrates, and 2.12 (1.31-3.35) for resins. After adjustment for confounding factors the adjusted odds ratios (95% CI) compared with controls were 0.69 (0.64-0.74) for statins, 0.60 (0.41-0.86) for ezetimibe, 0.87 (0.51-1.42) for fibrates, and 1.21 (0.69-2.06) for resins.
CONCLUSIONS: Use of statins and ezetimibe was inversely correlated with severe hyponatremia. Consequently, these drugs are unlikely culprits in patients with hyponatremia, and they appear safe to initiate in hyponatremic patients. A potential protective effect warrants further studies on how statins and other lipid-lowering drugs are linked to dysnatremias.

Many drugs used in psychiatry have been reported to cause hyponatraemia. However, lithium may be an exception due to its potential for causing nephrogenic diabetes insipidus, but clinical data are largely absent. The objective of this investigation was to study the association between lithium therapy and hospitalization due to hyponatraemia.
This study was a register-based case-control investigation of the general Swedish population. Patients hospitalized with a principal diagnosis of hyponatraemia (n=11,213) were compared with matched controls (n=44,801). Analyses using multivariable logistic regression adjusting for co-medication, diseases, previous hospitalizations and socioeconomic factors were deployed to calculate the association between severe hyponatraemia and the use of lithium. Additionally, newly initiated (⩽90 days) and ongoing lithium therapy was studied separately.
Compared with controls, the unadjusted odds ratio (OR) (95% confidence interval (CI)) for hospitalization due to hyponatraemia was 1.07 (0.70-1.59) for lithium. However, after adjustment for confounding factors the risk was reduced (adjusted OR: 0.53 (0.31-0.87)). Newly initiated lithium therapy was not significantly associated with hyponatraemia (adjusted OR 0.73 (0.35-5.38)). In contrast, for ongoing therapy the corresponding adjusted OR was significantly reduced (adjusted OR: 0.52 (0.30-0.87)).
A marked inverse association was found between ongoing lithium therapy and hospitalization due to hyponatraemia.

Calcium channel blockers (CCBs), beta-receptor blockers (BBs), angiotensin-converting enzyme inhibitors (ACEIs), and angiotensin II receptor blockers (ARBs) have occasionally been reported to cause severe hyponatremia. The aim was to explore the association between CCBs, BBs, ACEIs, and ARBs and hospitalization due to hyponatremia.
Patients hospitalized with a principal diagnosis of hyponatremia (n = 11 213) were compared with matched controls (n = 44 801). Linkage of national population-based registers was used to acquire data. Multivariable logistic regression adjusting for co-medications, diseases, previous hospitalizations, and socioeconomic factors was used to explore the association between hospitalization for severe hyponatremia and the use of different CCBs, BBs, ACEIs, and ARBs. Furthermore, newly initiated (≤90 days) and ongoing use were examined separately.
Adjusted odds ratios (aORs) (95% confidence interval) for the investigated 4 drug classes ranged from 0.86 (0.81-0.92) for CCBs to 1.15 (1.07-1.23) for ARBs. For newly initiated drugs, aORs spanned from 1.64 (1.35-1.98) for CCBs to 2.24 (1.87-2.68) for ACEIs. In contrast, the corresponding associations for ongoing therapy were not elevated, ranging from 0.81 (0.75-0.86) for CCBs to 1.08 (1.00-1.16) for ARBs. In the CCBs subgroups, aOR for newly initiated vascular CCBs was 1.95 (1.62-2.34) whereas aOR for ongoing treatment was 0.82 (0.77-0.88).
For newly initiated CCBs, BBs, ACEIs, and ARBs, the risk of hospitalization due to hyponatremia was moderately elevated. In contrast, there was no evidence that ongoing treatment with investigated antihypertensive drugs increased the risk for hospitalization due to hyponatremia.