Abnormal serum sodium levels are a common and severe complication in stroke patients, significantly increasing mortality risk and prolonging ICU stays. Accurate real-time prediction of serum sodium fluctuations is crucial for optimizing clinical interventions. However, existing predictive models face limitations in handling complex dynamic features and long time series data, making them less effective in guiding individualized treatment. To address this challenge, this study developed a deep learning model based on a multi-head attention mechanism to enable real-time prediction of serum sodium concentrations and provide personalized intervention recommendations for ICU stroke patients. This study utilized publicly available MIMIC-III (n = 2346) and MIMIC-IV (n = 896) datasets, extracting time series data from 10 key clinical indicators closely associated with serum sodium levels. To address the complexity of long time series data, a moving sliding window sub-sampling segmentation method was employed, effectively transforming extensive sequences into more manageable inputs while preserving critical temporal dependencies. By leveraging advanced mathematical modeling, meaningful insights were extracted from sparse and irregular time series data. The resulting time-feature fusion multi-head attention (TFF-MHA) model underwent rigorous validation using public datasets and demonstrated superior performance in predicting both serum sodium values and corresponding intervention measures compared to existing models. This study contributes to the field of healthcare informatics by introducing an innovative, data-driven approach for dynamic serum sodium prediction and intervention recommendation, providing a valuable clinical decision-support tool for optimizing sodium management strategies in critically ill stroke patients.

Chronic hyponatremia is common in hospitalized patients and associated with high mortality. To what extent this reflects a causal effect remains uncertain.

This study was based on the Stockholm Sodium Cohort, a longitudinal laboratory data repository covering 1.6 million individuals from 2005 to 2018. Using 1:1 propensity score matching, we explored mortality rates and causes of death in patients with mild (130-134 mmol/L), moderate (125-129 mmol/L), profound (120-124 mmol/L) or very profound (<120 mmol/L) hyponatremia compared to patients with normal (135-145 mmol/L) sodium concentrations on admittance to medical wards.

In total, 283 837 individuals fulfilled inclusion criteria, 79 407 of which had hyponatremia. Of these, 66 941 (52.7 % women) were successfully matched to counterparts with normal sodium concentrations. Thirty-day mortality rates were higher in patients with hyponatremia (HRs from 1.35 [95 % CI 1.28-1.42] in mild to 3.38 [95 % CI 2.16-5.28] in very profound hyponatremia). One-year mortality rates were marginally elevated in patients with mild hyponatremia (HR 1.04 [95 %CI 1.01-1.07]), but higher with more pronounced hyponatremia (HRs 1.18 [95 %CI 1.09-1.27] to 1.38 [95 %CI 1.11-1.69]). Excess 30-day mortality in mild, moderate, and profound hyponatremia was largely driven by malignant and gastrointestinal diseases.

Excess mortality with hyponatremia is proportional to the sodium disturbance but attenuates over time. However, causes of death suggest that residual confounding from imbalanced severity of underlying diseases is the main cause of increased mortality.

Water homeostasis is controlled by a brain-kidney axis that consists of central osmoreceptors, synthesis and secretion of arginine vasopressin (AVP) and AVP-responsive aquaporin-2 (AQP2) water channels in kidney collecting duct principal cells that facilitate water reabsorption. In addition to AVP, thirst represents a second line of defence to maintain water balance. Water balance disorders arise because of deficiency, resistance or inappropriate secretion of AVP or disturbances in thirst sensation (hypodipsia, polydipsia). People with water balance disorders are prone to develop hyponatraemia or hypernatraemia, which expose cells to osmotic stress and activate cell volume regulation mechanisms. This review covers several recent insights that have expanded our understanding of central osmoregulation, AQP2 regulation and cell volume regulation. This includes the role of with no lysine kinase 1 (WNK1) as a putative central osmolality sensor and, more generally, as an intracellular crowding sensor that coordinates the cell volume rescue response by activating sodium and potassium cotransporters. Furthermore, several new regulators of AQP2 have been identified, including AVP-dependent AQP2 regulation (yes-associated protein, nuclear factor of activated T-cells, microRNAs) and AVP-independent AQP2 regulation (epidermal growth factor receptor, fluconazole, prostaglandin E2). It is also becoming increasingly clear that long-term cell volume adaptation to chronic hypotonicity through release of organic osmolytes comes at the expense of compromised organ function. This potentially explains the complications of chronic hyponatraemia, including cognitive impairment, bone loss and vascular calcification. This review illustrates why these new insights derived from basic science are also relevant for developing new approaches to treat water balance disorders.

Lower dietary energy intake (DEI) may be associated with increased mortality risk. This study aims to analyze the influence of baseline DEI, time average DEI, and other factors on survival in peritoneal dialysis (PD) patients.

It was a single-center retrospective cohort study. Patients who started PD from January 2006 to June 2021 were included in this study and followed up until June 2023. Their baseline (six months after the beginning of PD) demographic, dietary intake, laboratory data, and time varying dietary intake data were collected and analyzed. The relationships between these data and survival were examined using Cox model to estimate death hazard ratios.

A total of 794 patients were included in this study, 424 males and 370 females, with a mean age of 58.87 ± 16.02 years. Their mean normalize baseline dietary energy intake (nDEI) was 25.46 ± 6.72 kcal/kg/day, time average nDEI was 24.87 ± 4.74 kcal/kg/day. The median follow-up duration was 46.58 (27.38, 78.52) months in the overall cohort. Based on multivariate Cox proportional hazard analysis, age (HR = 1.056, 95% Cl = 1.047-1.065, p < 0.001), diabetes (HR = 1.364, 95% Cl = 1.114-1.671, p = 0.003), serum albumin (HR = 0.945, 95% Cl = 0.923-0.967, p < 0.001), blood sodium (HR = 0.973, 95% Cl = 0.954-0.992, p = 0.002), serum urea (HR = 0.974, 95% Cl = 0.953-0.994, p = 0.025), and baseline nDEI (HR = 0.980, 95% Cl = 0.964-0.996, p = 0.017) were significantly associated with mortality. Baseline DPI, BMI and time average nDEI were not related to PD patients' survival. When classified baseline nDEI into 4 groups (< 25 kcal/kg/day, 25-29.99 kcal/kg/day, 30-34.99 kcal/kg/day, and ≥ 35 kcal/kg/day), the univariate and multivariate Cox proportional hazard analysis showed that the patients with nDEI 30-34.99 kcal/kg/day had the lowest mortality risk (using the DEI < 25 kcal/kg/day group as reference, p < 0.05).

Our study revealed that DEI 30-34.99 kcal/kg/day might be beneficial to the long-term outcome for the Chinese PD population.

Not applicable.

This review article series on water and electrolyte disorders is based on the 'Electrolyte Winter Seminar' held annually for young nephrologists in Japan. The seminar features dynamic case-based discussions, some of which are included as self-assessment questions in this series. The second article in this series focuses on treatment of hyponatremia, a common water and electrolyte disorder frequently encountered in clinical practice. Hyponatremia presents diagnostic challenges due to its various etiologies and the presence of co-morbidities that affect water and electrolyte homeostasis. Furthermore, limited evidence, including a lack of robust randomized controlled trials, complicates treatment decisions and increases the risk of poor outcomes from inappropriate management of both acute and chronic hyponatremia. This review provides a comprehensive overview of treatment of hyponatremia for better comprehension and improved clinical practice.

Hyponatremia is the most common electrolyte disorder, with potentially serious consequences. Studies validating hyponatremia used as a principal diagnosis are lacking. Studying principal diagnoses is important since it indicates the main reason for inpatient care. The aim of this study was to assess the validity of principal diagnoses of hyponatremia according to the International Classification of Diseases, tenth revision (ICD-10) in patients discharged from hospital.

Three independent reviewers retrospectively analyzed medical records of 428 hospitalized patients, ≥18 years old, discharged with a principal diagnosis of either hyponatremia or syndrome of inappropriate anti-diuretic hormone secretion (SIADH) from three different hospitals during 2014-2017. The positive predictive value of hyponatremia as a principal diagnosis was calculated.

The median age of the studied population was 73 (IQR 64-81) years and 69% were women. The range of sodium levels was < 100 to 139 mmol/L. The mean sodium level was 119 mmol/L. Of the patients 27% were treated in an intensive care unit (ICU)/high dependency unit (HDU). Hyponatremia was deemed to be the principal cause of inpatient care in 411 out of 428 patients, corresponding to a positive predictive value for hyponatremia as a principal diagnosis of 96% (CI 95% 94-98).

The current study showed that 19 diagnoses out of 20 were correct implying a high validity. Thus, a principal diagnosis of hyponatremia, appears to be a useful measure in clinical and epidemiological studies aiming to target a clinically relevant consequence of hyponatremia in hospitalized patients.

The 72-h emergency department (ED) revisit rate is a key quality indicator. While some revisits stem from medical errors or inadequate initial treatment, others are due to disease progression or a lack of accessible care. The development of a risk assessment tool could identify high-risk patients and improve resource management.

This study was conducted via an electronic health records system at a tertiary center in Taiwan. We derived a risk model via logistic regression and bootstrapping methods using a retrospective cohort of adults who underwent 72-h ED revisits between January 2019 and December 2020. The study population was divided into development (2019: 1224) and validation datasets (2020: 985). The primary outcome was high-risk return, defined as intensive care unit (ICU) admission or in-hospital mortality after 72-h ED return.

On the basis of the odds ratio, eight variables were independently associated with high-risk ED returns and subsequently included in the HANDLE-24 score (hypertension; symptoms of acute coronary syndrome; dysnatremia; dyspnea; liver disease; triage level escalation; and revisits within 24 h). The area under the receiver operating characteristic curve was 0.816 (95% CI: 0.760-0.871, p < 0.001) in the development dataset and 0.804 (0.750-0.858) in the validation dataset. Patients can be divided into three risk categories on the basis of the HANDLE-24 score: low [0-8.5], moderate [9-11.5] and high [12-22] risk groups. The ability of our risk score to predict the rates of hospital admission, ICU admission and in-hospital mortality was significant according to the Cochran‒Armitage trend test.

The HANDLE-24 score represents a simple tool that allows early risk stratification and suggests more aggressive therapeutic strategies for patients experiencing ED revisits. The risk of adverse outcomes in ED adults after revisiting can be swiftly assessed via easily available information.

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a complex and often underdiagnosed disorder characterized by impaired water homeostasis, leading to hyponatremia and associated complications. This comprehensive review explores the intersection of SIADH with chronic respiratory diseases, including chronic obstructive pulmonary disease (COPD), pulmonary tuberculosis, cystic fibrosis, and interstitial lung disease. The review looks at current evidence on pathophysiology, diagnostic challenges, and treatment approaches, highlighting the need for specialized management strategies to improve patient outcomes. Through an analysis of clinical and observational studies, this review highlights the significant impact of SIADH on morbidity and mortality among patients with respiratory diseases. It illustrates the necessity for further research to refine diagnostic and therapeutic modalities.

The study aimed to assess the impact of varying degrees of initial serum sodium change among patients with type 2 diabetes (T2D) starting sodium-glucose cotransporter-2 inhibitor (SGLT2i) therapy and their subsequent clinical outcome.

We used medical data from a multicentre health care provider in Taiwan and recruited 4400 patients with T2D with baseline normal serum sodium (135-145 mmol/L) and follow-up serum sodium measures available after 3 months of SGLT2i treatment from 1 June 2016 to 31 December 2021.

After a median of 2.9 (2.4, 3.4) months of SGLT2i treatment, overall, there was a minimal change in serum sodium levels (from 139.6 ± 2.4 to 139.5 ± 3.7 mmol/L). Most patients (87.8%) maintained normal sodium levels, while 8.6% (n = 378) experienced hyponatraemia (<135 mmol/L) and 3.6% (n = 158) hypernatraemia (>145 mmol/L). Factors independently associated with hyponatraemia included cancer history, chronic lung disease, insulin use, higher glycated haemoglobin, impaired liver function, lower baseline sodium and greater initial decline in kidney function. Conversely, factors linked to hypernatraemia included older age, absence of cancer history, loop diuretic and non-steroidal anti-inflammatory drug use, higher baseline sodium and a lesser initial decline in kidney function. Over a median of 26.0 months of follow-up, hyponatraemia shortly after starting SGLT2i therapy was associated with significantly increased risks of major adverse cardiovascular events [hazard ratio (HR): 2.52; 95% confidence interval (CI): 1.83-3.48], heart failure for hospitalization (HR: 1.66; 95% CI: 1.16-2.37), major adverse renal events (HR: 2.27; 95% CI: 1.73-2.96) and all-cause death (HR: 2.98; 95% CI: 2.17-4.11) after adjusting for clinically relevant factors. Non-linear analysis indicated that a more pronounced initial decline in serum sodium levels correlated steeply with higher risks of these adverse events.

While most patients with T2D maintain stable serum sodium homeostasis on SGLT2i therapy, a subset may experience dysnatraemic events with potential worse clinical consequences. Physicians should be vigilant about monitoring sodium levels and considering the associated risks when initiating SGLT2i therapy in patients with risk.

Previous study consistently showed that lower serum sodium (SNa) was associated with a greater risk of mortality in hemodialysis (HD) patients. However, few studies have focused on the change in SNa (ΔSNa = post-HD SNa - pre-HD SNa) during an HD session.

In a retrospective cohort of maintenance HD adults, all-cause mortality and cardio-cerebrovascular event (CCVE) were followed up for a medium of 82 months. Baseline pre-HD SNa and ΔSNa were collected; time-averaged pre-HD SNa and ΔSNa were computed as the mean values within 1-year, 2-year and 3-year intervals after enrollment. Cox proportional hazards models were used to evaluate the relationships of pre-HD and ΔSNa with outcomes.

Time-averaged pre-HD SNa were associated with all-cause mortality (2-year pre-HD SNa: HR [95% CI] 0.86 [0.74-0.99], p = 0.042) and CCVE (3-year pre-HD SNa: HR [95% CI] 0.83 [0.72-0.96], p = 0.012) with full adjustment. Time-averaged ΔSNa also demonstrated an association with all-cause mortality (3-year ΔSNa: HR [95% CI] 1.26 [1.03-1.55], p = 0.026) as well as with CCVE (3-year ΔSNa: HR [95% CI] 1.51 [1.21-1.88], p = <0.001) when fully adjusted. Baseline pre-HD SNa and ΔSNa didn't exhibit association with both outcomes.

Lower time-averaged pre-HD SNa and higher time-averaged ΔSNa were associated with a greater risk of all-cause mortality and CCVE in HD patients.

Cardiovascular (CV) disease is the leading cause of death in dialysis patients and is strongly associated with fluid overload and hypertension. It is plausible that low dialysate sodium ion concentration [Na+] may decrease total body sodium content, thereby reducing fluid overload and hypertension and ultimately reducing CV morbidity and death. This is an update of a review first published in 2019.

This review evaluated the harms and benefits of using a low (< 138 mM) dialysate [Na+] for maintenance haemodialysis (HD) patients.

We searched the Cochrane Kidney and Transplant Register of Studies up to 1 October 2024 through contact with the Information Specialist using search terms relevant to this review. Studies in the Register are identified through searches of CENTRAL, MEDLINE, and EMBASE, conference proceedings, the International Clinical Trials Registry Platform (ICTRP) Search Portal and ClinicalTrials.gov.

Randomised controlled trials (RCTs), both parallel and cross-over, of low (< 138 mM) versus neutral (138 to 140 mM) or high (> 140 mM) dialysate [Na+] for maintenance HD patients were included.

Two authors independently screened studies for inclusion and extracted data. Statistical analyses were performed using the random-effects model, and results expressed as risk ratios (RR) for dichotomous outcomes, and mean differences (MD) or standardised MD (SMD) for continuous outcomes, with 95% confidence intervals (CI). Confidence in the evidence was assessed using Grades of Recommendation, Assessment, Development and Evaluation (GRADE).

We included 17 studies randomising 509 patients, with data available for 452 patients after dropouts. All but three studies evaluated a fixed concentration of low dialysate [Na+], with one using profiled dialysate [Na+] and two using individualised dialysate [Na+]. Five were parallel group studies, and 12 were cross-over studies. Of the latter, only six used a washout between intervention and control periods. Most studies were short-term with a median (interquartile range) follow-up of 4 (4 to 16) weeks. Two were of a single HD session and two of a single week's HD. Seven studies were conducted prior to 2000, and six reported the use of obsolete HD practices. Other than for indirectness arising from older studies, risks of bias in the included studies were generally low. Compared to neutral or high dialysate [Na+] (≥ 138 mM), low dialysate [Na+] (< 138 mM) reduces interdialytic weight gain (14 studies, 515 participants: MD -0.36 kg, 95% CI -0.50 to -0.22; high certainty evidence) and antihypertensive medication use (5 studies, 241 participants: SMD -0.37, 95% CI -0.64 to -0.1; high certainty evidence), and probably reduces left ventricular mass index (2 studies, 143 participants: MD -7.65 g/m2, 95% CI -14.48 to -0.83; moderate certainty evidence), predialysis mean arterial pressure (MAP) (5 studies, 232 participants: MD -3.39 mm Hg, 95% CI -5.17 to -1.61; moderate certainty evidence), postdialysis MAP (5 studies, 226 participants: MD -3.17 mm Hg, 95% CI -4.68 to 1.67; moderate certainty evidence), predialysis serum [Na+] (11 studies, 435 participants: MD -1.26 mM, 95% CI -1.81 to -0.72; moderate certainty evidence) and postdialysis serum [Na+] (6 studies, 188 participants: MD -3.09 mM, 95% CI -4.29 to -1.88; moderate certainty evidence). Compared to neutral or high dialysate [Na+], low dialysate [Na+] probably increases intradialytic hypotension events (13 studies, 15,764 HD sessions: RR 1.58, 95% 1.25 to 2.01; moderate certainty evidence) and intradialytic cramps (10 studies, 14,559 HD sessions: RR 1.84, 95% 1.29 to 2.64; moderate certainty evidence). Effect size for important outcomes were generally greater with low dialysate [Na+] compared to high compared with neutral dialysate [Na+], although formal hypothesis testing identifies that the difference was only certain for postdialysis serum [Na+]. Compared to neutral or high dialysate [Na+], it is uncertain whether low dialysate [Na+] affects intradialytic or interdialytic MAP, and dietary salt intake. It is also uncertain whether low dialysate [Na+] changed extracellular fluid status, venous tone, arterial vascular resistance, left ventricular volumes, or fatigue. Studies did not examine CV or all-cause death, CV events, or hospitalisation.

Low dialysate [Na+] reduces intradialytic weight gain and probably blood pressure, which are effects directionally associated with improved outcomes. However, the intervention probably increases intradialytic hypotension and probably reduces serum [Na+], effects that are associated with an increased risk of death. The effect of the intervention on overall patient health and well-being is unknown. Further evidence is needed in the form of longer-term studies in contemporary settings, evaluating end-organ effects in small-scale mechanistic studies using optimal methods, and clinical outcomes in large-scale multicentre RCTs.

Abnormal fluid and plasma sodium concentrations are established prognostic factors for patients on hemodialysis. However, the cumulative effects of abnormal salt and water and potential effect modifications and the effect of dialysate sodium remain incompletely understood.

The study followed 68,196 patients on incident hemodialysis from 875 dialysis clinics in 25 countries over 10 years (2010–2020) investigating dose-response patterns between cumulative exposure time of fluid overload/depletion (measured by bioimpedance spectroscopy using the Fresenius Body Composition Monitor), abnormal plasma sodium levels, low dialysate sodium, and all-cause mortality. We calculated time-varying cumulative exposure (in months) of relative fluid overload (any degree; >7% or severe; >13 or >15% in women or men, respectively) and fluid depletion (<−7%), hypo- or hypernatremia (sodium <135 or >145 mmol/L, respectively), low dialysate sodium (≤138 mmol/L), and estimated hazard ratios for all-cause mortality using a multivariable Cox model.

Of 2,123,957 patient-months, 61% were spent in any degree of fluid overload, 4% in fluid depletion, 11% in hyponatremia, and 1% in hypernatremia. Any degree of fluid overload was associated with higher all-cause mortality (hazard ratio peak at 3.42 [95% confidence intervals, 3.12 to 3.75] relative to no exposure), and this association with all-cause mortality seemed to be stronger with severe fluid overload. The risk pattern associated with hyponatremia was approximately linear in the first four patient-months and then plateaued after the fourth patient-month. We did not observe effect modification between fluid overload and hyponatremia.

Even mild fluid overload was associated with higher mortality in patients on hemodialysis. Whether more stringent fluid management results in clinical improvement requires further investigation.

Hyponatraemia is a prevalent electrolyte disturbance observed in critically ill patients. The rapid correction of low plasma sodium levels by continuous renal replacement therapy (CRRT) carries the risk of developing osmotic demyelination syndrome (ODS), which can be prevented by implementing an individualized CRRT method.

This study aims to introduce a CRRT protocol for the safe and gradual correction of severe hyponatraemia.

This retrospective case series study was conducted in an intensive care unit (ICU). All four patients with severe hyponatraemia (<125 mmol/L) and renal failure between October 1, 2022, and September 30, 2023, were treated by CRRT with sterile water and regional citrate anticoagulation (RCA). Data on patient demographics, laboratory biochemical parameters, urine outputs and CRRT-related adverse events were collected. Laboratory parameters and urine outputs were compared by paired t-tests before and after CRRT.

After CRRT, sodium levels were significantly increased (112.7 ± 6.7 vs. 141.9 ± 2.8 mmol/L, p = .005). Abnormal urine outputs, potassium, creatinine and bicarbonate were corrected (p for all <.05). Safe and gradual correction of hyponatraemia and internal environmental dysregulation was achieved in all patients without any complications related to CRRT, particularly ODS.

It is a novel and simple strategy to correct severe hyponatraemia effectively while ensuring the safety of patients that can be easily implemented by experienced nurse staff.

The sterile water-based protocol for postfilter dilution is safe to correct severe hyponatraemia with RCA and can be easily performed by experienced critical care nurses according to the precalculated formula. CRRT-trained, experienced ICU nurses are competent to initiate and adjust sterile water infusion discretely to prevent overcorrection of hyponatraemia.

Disorders of serum sodium are common among general patients and are associated with poor outcomes. The prognostic value of serum sodium disorders in patients with acute pancreatitis (AP) has not been studied. We conducted this retrospective study to explore the association between serum sodium levels and the outcomes of patients with AP.

Patients with AP from the Medical Information Mart for Intensive Care III (MIMIC-III) were screened for this study. The laboratory variables, including serum sodium levels, were obtained by analyzing the first blood sample on the first day after admission. Univariate logistic regression was performed to discover potential factors for mortality of AP. The unadjusted and adjusted association between serum sodium level and mortality of AP was shown by the restricted cubic spline (RCS). The categorical cutoff for the detrimental effect of serum sodium level on the prognosis of AP was also confirmed by stepwise logistic regression after adjusting for con-founding effects of significant factors in the univariate logistic regression.

A total of 869 patients with AP in the MIMIC-III were included with a mortality of 13.1%. Unadjusted logistic regression showed that age (p < 0.001), simplified acute physiological score (SAPS) (p < 0.001), systolic blood pressure (p < 0.001), diastolic blood pressure (p < 0.001), hemoglobin (p = 0.040), serum creatinine (p = 0.046), and serum phosphorus (p < 0.001) were significantly associated with the mortality of AP. The RCS showed that the serum sodium level was negatively and linearly associated with mortality of AP after adjusting for confounding effects of significant factors in the univariate logistic regression. Serum sodium < 133 mmol/L, which indicated hyponatremia, was significantly correlated with a higher mortality risk than serum sodium ≥ 133 mmol/L (p = 0.013).

Hyponatremia is widely developed among patients with AP and correlates with a higher mortality risk of AP. Physicians should pay more attention to managing patients with AP with hyponatremia.

Dysnatremia is the most common electrolyte disorder in hospitalized patients. Sodium fluctuation level may be a better parameter in dysnatremia management. We aimed to examine the association between sodium fluctuation level during hospitalization and mortality and to evaluate its value in predicting poor prognosis among general hospitalized patients.

Data were collected from patients admitted to Peking Union Medical College Hospital. The generalized estimated equation (GEE) was used to examine the relationship between sodium fluctuation level and mortality. Receiver-operating characteristic (ROC) curve analysis was performed to calculate the optimal cutoff value and the area under the ROC curve (AUC).

Sodium fluctuation level showed a dose-dependent association with increased mortality in general hospitalized patients. After adjusting age, sex, length of hospital stay, and Charlson comorbidity index, the ORs of group G2 to G6 were 5.92 (95% CI 5.16-6.79), 26.45 (95% CI 22.68-30.86), 50.71 (95% CI 41.78-61.55), 104.38 (95% CI 81.57-133.58), and 157.64 (95% CI 112.83-220.24), respectively, p trend <0.001. Both normonatremia and dysnatremia patients on admission had the dose-dependent associations similar to general hospitalized patients. The AUC of sodium fluctuation level was 0.868 (95% CI 0.859-0.877) in general hospitalized patients, with an optimal cutoff point of 7.5 mmol/L, a sensitivity of 76.5% and a specificity of 84.2%.

We determined that sodium fluctuation level had a dose-dependent association with increased mortality in general hospitalized patients. Sodium fluctuation level could be used to develop a single parameter system in predicting mortality in general hospitalized patients with acceptable accuracy, sensitivity, and specificity.

Mild hyponatremia is often found in patients visiting pediatric emergency departments (PEDs), but there are few large-scale studies on its association with adverse outcomes, including mortality. We conducted this study to identify the association of mild hyponatremia with adverse outcome. This retrospective observational study included children under 18 years of age visiting the PED at a tertiary hospital. We used electronic medical record data from January 1, 2009 to December 31, 2020. Clinical outcomes, including ward admission, vasopressor administration, pediatric intensive care unit (PICU) admission, and mortality, were assessed for the total of 44,147 patients. Among these, 1,639 (3.7%) were in the hyponatremia group, with 1,521 (3.4%) exhibiting mild hyponatremia. Mild hyponatremia was more prevalent in younger patients, particularly in the 1-3 years age group, and less common in females. Patients with mild hyponatremia had a significantly prolonged median length of stay in the PED compared to normonatremic patients (5.8 h vs. 4.4 h, p < 0.001). Moreover, they showed significantly higher rates of ward admission (51.1% vs. 35.6%, p < 0.001), vasopressor administration (1.1% vs. 0.6%, p = 0.014), PICU admission (2.4% vs. 1.0%, p < 0.001), and mortality (1.5% vs. 0.3%, p < 0.001). Compared with the normonatremia group, the odds ratios (95% CI) for ward admission, vasopressor administration, PICU admission, and mortality in the mild hyponatremia group were 1.90 (1.71-2.10), 1.91 (1.17-3.13), 2.62 (1.86-3.68), and 5.56 (3.51-8.80), respectively. Furthermore, our findings demonstrate a notable upward trend in adverse outcomes, including vasopressor administration, PICU admission, and mortality, from mild hyponatremia to severe hyponatremia. In conclusion, we found that adverse outcomes increase with the severity of hyponatremia in children presenting to the PED, highlighting the importance of immediate intervention alongside the identification of the underlying cause.

Hyponatremia is the most common electrolyte disorder often present in peritoneal dialysis (PD) patients. The aim of this retrospective study was to investigate the effect of hyponatremia on mortality in patients undergoing PD.

The health records of adult individuals with an inserted PD catheter identified via the centralized national e-health database were used.

The mean age of the 846 patients included in the study was 52.48 years (±14.6). The mean sodium level was 136.51 mEq/L. Sodium levels <137 mEq/L were associated with higher death risk independent of comorbidities. There was a 0.821 times less reduction in mortality for each mEq /L increase in serum sodium.

Our study provides evidence that monitoring and adjusting serum sodium levels is crucial in managing PD patients with hyponatremia, as low serum sodium level was found to be a significant and independent predictor of mortality.

Background: Sodium fluctuation is independently associated with clinical deterioration. We developed and validated a prognostic index based on sodium fluctuation for risk stratification and in-hospital monitoring. Methods: This study included 33,323 adult patients hospitalized at a tertiary care hospital in 2014. The first 28,279 hospitalizations were analyzed to develop the model and then the validity of the model was tested using data from 5044 subsequent hospitalizations. We predict in-hospital mortality using age, comorbidity, range of sodium fluctuation, and duration of sodium fluctuation, abbreviated as CARDS. Results: In-hospital mortality was similar in the derivation (0.6%) and validation (0.4%) cohorts. In the derivation cohort, four independent risk factors for mortality were identified using logistic regression: age (66-75, 2 points; >75, 3 points); Charlson comorbidity index (>2, 5 points); range of sodium fluctuation (7-10, 4 points; >10, 10 points); and duration of fluctuation (≤3, 3 points). The AUC was 0.907 (95% CI: 0.885-0.928) in the derivation cohort and 0.932 (95% CI: 0.895-0.970) in the validation cohort. In the derivation cohort, in-hospital mortality was 0.106% in the low-risk group (0-7 points), 1.076% in the intermediate-risk group (8-14 points), and 8.463% in the high-risk group (15-21 points). In the validation cohort, in-hospital mortality was 0.049% in the low-risk group, 1.064% in the intermediate-risk group, and 8.403% in the high-risk group. Conclusions: These results suggest that patients at low, intermediate, and high risk for in-hospital mortality may be identified by CARDS mainly based on sodium fluctuation.

Hyponatremia is associated with considerable morbidity and mortality, but causal links have been difficult to establish. Here, we describe the establishment and representativeness of the Stockholm Sodium Cohort (SSC), designed to study etiologies and outcomes of hyponatremia.

All residents of Stockholm County undertaking at least one serum sodium test between 2005-2018 were included in the SSC. Individual-level test results from over 100 laboratory parameters relevant to hyponatremia were collected and linked to data on demographics, socioeconomic status, healthcare contacts, diagnoses and dispensed prescription medications using national registers.

A total of 1,632,249 individuals, corresponding to 64% of the population of Stockholm County, were included in the SSC. Coverage increased with advancing age, ranging from 32% in children and adolescents (≤18 years) to 97% among the oldest (≥80 years). The coverage of SSC included the vast majority of patients in Stockholm County diagnosed with diabetes mellitus (93%), myocardial infarction (98%), ischemic stroke (97%), cancer (85%), pneumonias requiring inpatient care (95%) and deaths (88%).

SSC is the first cohort specifically designed to investigate sodium levels in a large, population-based setting. It includes a wide range of administrative health data and laboratory analyses. The coverage is high, particularly among elderly and individuals with comorbidities. Consequently, the cohort has a large potential for exploration of various aspects of hyponatremia.

Hyponatremia is a disorder of water homeostasis. Water balance is maintained by the collaboration of renal function and cerebral structures, which regulate thirst mechanisms and secretion of the antidiuretic hormone. Measurement of serum-osmolality, urine osmolality and urine-sodium concentration help to diagnose the different reasons for hyponatremia. Hyponatremia induces cerebral edema and might lead to severe neurological symptoms, which need acute therapy. Also, mild forms of hyponatremia should be treated causally, or at least symptomatically. An inadequate fast increase of the serum sodium level should be avoided, because it raises the risk of cerebral osmotic demyelination. Basic pathophysiological knowledge is necessary to identify the different reasons for hyponatremia which need different therapeutic procedures.

Hyponatremia is a common electrolyte disturbance in patients with neurological disease; however, its predictive role for outcome in patients with supratentorial spontaneous intracerebral hemorrhage (sICH) is controversial. This study aims to explore the association between hyponatremia within 7 days after bleeding and 90-day mortality in patients with supratentorial sICH.

A retrospective analysis was conducted at our institution. Patients with sICH meeting the inclusion criteria were enrolled in this study. Multivariate regression analyses were performed to determine the predictive value of hyponatremia (serum sodium <135 mmol/L) for 90-day mortality and functional outcome. Subgroup analysis was performed based on the degree and duration of hyponatremia and therapeutic strategies. The Spearman correlation test was performed to explore the relationship between hyponatremia severity and duration with variables in a multivariate regression model. Kaplan-Meier curve was depicted to reveal the relationship between hyponatremia and mortality. The receiver operating characteristic (ROC) curve was plotted to show the diagnostic effect of the minimum concentration of serum sodium (sodiummin) on 90-day mortality.

A total of 960 patients were enrolled, 19.6% (188) of whom were patients with hyponatremia and 26.0% (250) had 90-day mortality. The incidence of hyponatremia was roughly 2.5 times in non-survivors compared with survivors (34.8% vs. 14.2%). Multivariate regression analysis revealed that hyponatremia was the independent predictor of 90-day mortality (OR 2.763, 95%CI 1.836-4.157) and adverse outcome (OR 3.579, 95%CI 2.332-6.780). Subgroup analysis indicated an increased trend in mortality risk with both duration (more or less than 48 h) and severity of hyponatremia (mild, moderate, and severe) and confirmed the predictive value of hyponatremia for mortality in patients undergoing surgical intervention (external ventricular drainage, craniotomy, and decompressive craniectomy; all p < 0.05). The Spearman correlation test indicated no moderate or strong relationship between hyponatremia severity and duration with other variables in the multivariate model (all |rs| < 0.4). The ROC curve suggested the moderate diagnostic performance of sodiummin for mortality in both general patients and subgroups of therapeutic method patients (AUC from 0.6475 to 0.7384).

Hyponatremia occurring in the first 7 days after bleeding is an independent predictor of 90-day morality and adverse outcome. Rigorous electrolyte scrutiny in patients treated surgically is required.

Hyponatremia on admission has been related to worse outcomes in patients with COVID-19 infection. However, little is known about the frequency and the associated risk factors of hyponatremia after COVID-19 discharge. We performed an observational 24-month follow-up study of patients admitted during the first COVID-19 wave. Kaplan-Meier curves and Cox proportional hazard models were used to assess the main variables in predicting hyponatremia on follow-up (HYPO-FU). A total of 161 out of 683 (24.4%) developed HYPO-FU. The group with HYPO-FU comprised of more men [(62.3%) vs. (49.2%); p < 0.01], older [65.6 ± 18.2 vs. 60.3 ± 17.0; p < 0.01] and more frequently re-admitted [(16.2%) vs. (3.8%); p < 0.01). The rate of HYPO-FU was higher in the first year 23.6 per 100 individuals per year. After Cox regression analysis, the independent risk factors of HYPO-FU were diabetes [OR 2.12, IC 95% (1.48-3.04)], hypertension [OR 2.18, IC 95% (1.53-3.12)], heart failure [OR 3.34, IC 95% (1.72-6.48)] and invasive ventilation support requirement [OR: 2.38, IC 95% (1.63-3.50)]. To conclude, HYPO-FU was frequent in the first year after COVID-19 infection, and the risk was higher in older men with comorbidities, increasing rehospitalisation. Further studies aimed at evaluating the beneficial effects of correcting hyponatremia in these patients are warranted.

Hyponatremia is a common and important electrolyte disorder. However, the prevalence and factors associated with hyponatremia in patients with chronic kidney disease (CKD) are unknown.

We studied the factors associated with hyponatremia (< 135 mEq/L) in CKD patients registered in the Fukuoka Kidney Disease Registry (FKR) study using a logistic regression model variable selected using the variable reduction method.

We analyzed the baseline characteristics of 4367 participants with CKD (age, 64 ± 16 years; male, 56.1%). Hyponatremia was detected in 2.0% of the patients at baseline, and multivariate logistic analysis showed that the independent factors for hyponatremia were body mass index (odds ratio [OR] 0.91; 95% confidence interval [CI] 0.85-0.97), prescription of benzodiazepine (OR 2.31; 95% CI 1.39-3.86), blood hemoglobin level (OR 0.76; 95% CI 0.65-0.88), and serum C-reactive protein level (OR 1.27; 95% CI 1.04-1.54).

The cross-sectional analysis using baseline data from the FKR study revealed independent factors associated with hyponatremia in patients with decreased kidney function. Longitudinal analyses of the FKR cohort are needed to evaluate the effects of these factors on the prognosis of hyponatremia in patients with CKD.

Assessing regional wall motion abnormalities (RWMA) in the myocardium may provide early diagnosis and treat chronic remodeling in STEMI patients. We assessed RWMA in 217 subjects with anterior STEMI admitted to Era University Hospital in Lucknow, UP, India. Besides abnormalities in the LAD territory, sub-sets of patients exhibited diffuse regional myocardial dysfunction. Interestingly, variations in serum electrolytes, specifically sodium and potassium, significantly affected the distribution and frequency of RWMA. Notably, RWMA occurred in the basal septum, apical septum, apex, and lateral wall in the anterior STEMI group. Additionally, the rate of regional dysfunction varied with serum urea and creatinine levels. This suggests that anterior STEMI can manifest myocardial abnormalities beyond the LAD territory. These findings indicate that ST-segment elevation might not be specific, possibly influenced by electrolyte changes affecting cardiac rhythm. Therefore, diagnosing and correcting region-specific wall motion abnormalities and electrolyte imbalances may improve outcomes in STEMI patients.

The 5-year mortality rate for haemodialysis patients is over 50%. Acute and chronic disturbances in salt and fluid homeostasis contribute to poor survival and are established as individual mortality risk factors. However, their interaction in relation to mortality is unclear.

We used the European Clinical Database 5 to investigate in a retrospective cohort analysis the relationship between transient hypo- and hypernatremia, fluid status and mortality risk of 72 163 haemodialysis patients from 25 countries. Incident haemodialysis patients with at least one valid measurement of bioimpedance spectroscopy were followed until death or administrative censoring from 1 January 2010 to 4 December 2019. Fluid overload and depletion were defined as >2.5 L above, and -1.1 L below normal fluid status, respectively. N = 2 272 041 recorded plasma sodium and fluid status measurements were available over a monthly time grid and analysed in a Cox regression model for time-to-death.

Mortality risk of hyponatremia (plasma sodium <135 mmol/L) was slightly increased when fluid status was normal [hazard ratio (HR) 1.26, 95% confidence interval (CI) 1.18-1.35], increased by half when patients were fluid depleted (HR 1.56, 95% CI 1.27-1.93) and accelerated during fluid overload (HR 1.97, 95% CI 1.82-2.12).

Plasma sodium and fluid status act independently as risk factors on mortality. Patient surveillance of fluid status is especially important in the high-risk subpopulation of patients with hyponatremia. Prospective patient-level studies should examine the effects of chronic hypo- and hypernatremia, risk determinants, and their outcome risk.

The utilization of vasopressin receptor antagonists, known as vaptans, in the management of hyponatremia among patients afflicted with the syndrome of inappropriate antidiuretic hormone (SIADH) remains a contentious subject. This meta-analysis aimed to evaluate the safety and efficacy of vaptans for treating chronic hyponatremia in adult SIADH patients. Clinical trials and observational studies were identified by a systematic search using MEDLINE, EMBASE, and Cochrane Database from inception through September 2022. The inclusion criteria were the studies that reported vaptans' safety or efficacy outcomes compared to placebo or standard therapies. The study protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO; CRD 42022357307). Five studies were identified, comprising three RCTs and two cohort studies, enrolling a total of 1840 participants. Regarding short-term efficacy on days 4-5, vaptans exhibited a significant increase in serum sodium concentration from the baseline in comparison to the control group, with a weighted mean difference of 4.77 mmol/L (95% CI, 3.57, 5.96; I2 = 34%). In terms of safety outcomes, the pooled incidence rates of overcorrection were 13.1% (95% CI 4.3, 33.6; I2 = 92%) in the vaptans group and 3.3% (95% CI 1.6, 6.6; I2 = 27%) in the control group. Despite the higher correction rate linked to vaptans, with an OR of 5.72 (95% CI 3.38, 9.70; I2 = 0%), no cases of osmotic demyelination syndrome were observed. Our meta-analysis comprehensively summarizes the efficacy and effect size of vaptans in managing SIADH. While vaptans effectively raise the serum sodium concentration compared to placebo/fluid restriction, clinicians should exercise caution regarding the potential for overcorrection.

Abnormalities of serum sodium are associated with increased mortality risk in hospitalised patients, but it is unclear whether, and to what extent other factors influence this relationship. We investigated the impact of dysnatraemia on total and cause-specific mortality in the Irish health system while exploring the concurrent impact of age, kidney function and designated clinical work-based settings.

A retrospective cohort study of 32,666 participants was conducted using data from the National Kidney Disease Surveillance System. Hyponatraemia was defined as < 135 mmol/L and hypernatraemia as > 145 mmol/L with normal range 135-145 mmol/L. Multivariable Cox proportional hazards regression was used to estimate hazard ratios (HR's) and 95% Confidence Intervals (CIs) while penalised spline models further examined patterns of risk.

There were 5,114 deaths (15.7%) over a median follow up of 5.5 years. Dysnatraemia was present in 8.5% of patients overall. In multivariable analysis, both baseline and time-dependent serum sodium concentrations exhibited a U-shaped association with mortality. Hyponatremia was significantly associated with increased risk for cardiovascular [HR 1.38 (1.18-1.61)], malignant [HR: 2.49 (2.23-2.78)] and non-cardiovascular/non-malignant causes of death [1.36 (1.17-1.58)], while hypernatremia was significantly associated with cardiovascular [HR: 2.16 (1.58-2.96)] and non-cardiovascular/ non-malignant deaths respectively [HR: 3.60 (2.87-4.52)]. The sodium-mortality relationship was significantly influenced by age, level of kidney function and the clinical setting at baseline (P < 0.001). For hyponatraemia, relative mortality risks were significantly higher for younger patients (interaction term P < 0.001), for patients with better kidney function, and for patients attending general practice [HR 2.70 (2.15-3.36)] than other clinical settings. For hypernatraemia, age and kidney function remained significant effect modifiers, with patients attending outpatient departments experiencing the greatest risk [HR 9.84 (4.88-18.62)] than patients who attended other clinical locations. Optimal serum sodium thresholds for mortality varied by level of kidney function with a flattening of mortality curve observed for patients with poorer kidney function.

Serum sodium concentrations outside the standard normal range adversly impact mortality and are associated with specific causes of death. The thresholds at which these risks appear to vary by age, level of kidney function, and are modified in specific clinical settings within the health system.

The complex classification for the diagnosis and treatment illustrates that hyponatremia is a very heterogeneous disorder. However, data on hyponatremia induced by flecainide, an often-prescribed antiarrhythmic agent, are scarce in the literature. A 78-year-old man with a recent history of recurrent hyponatremia and symptomatic paroxysmal atrial fibrillation presented with the complaints of dizziness and fatigue. During his repeated hospital admissions, the patient was treated with hypertonic saline, which temporarily improved serum sodium levels, but hyponatremia recurred without sustained clinical improvement. After discontinuation of the drug, the sodium levels remained stable. Doctors should be aware of not only the electrocardiographic changes associated with flecainide, but also the less-often found clinical manifestations linked with hyponatremia.

Hyponatremia is one of the most common problems encountered in clinical practice and one of the least-understood because accurate diagnosis and management require some familiarity with water homeostasis physiology, making the topic seemingly complex. The prevalence of hyponatremia depends on the nature of the population studied and the criteria used to define it. Hyponatremia is associated with poor outcomes including increased mortality and morbidity. The pathogenesis of hypotonic hyponatremia involves the accumulation of electrolyte-free water caused by either increased intake and/or decrease in kidney excretion. Plasma osmolality, urine osmolality, and urine sodium can help to differentiate among the different etiologies. Brain adaptation to plasma hypotonicity consisting of solute extrusion to mitigate further water influx into brain cells best explains the clinical manifestations of hyponatremia. Acute hyponatremia has an onset within 48 hours, commonly resulting in severe symptoms, while chronic hyponatremia develops over 48 hours and usually is pauci-symptomatic. However, the latter increases the risk of osmotic demyelination syndrome if hyponatremia is corrected rapidly; therefore, extreme caution must be exercised when correcting plasma sodium. Management strategies depend on the presence of symptoms and the cause of hyponatremia and are discussed in this review.

This article will discuss the consequences of chronic hyponatremia. In conditions such as cancer, heart failure, liver cirrhosis, or chronic kidney disease, the presence and magnitude of hypotonic hyponatremia are considered to reflect the severity of the underlying disease and are associated with increased morbidity as well as mortality. Hyponatremia can be acute (<48 h) or chronic (>2-3 days). Chronic hyponatremia is associated with attention deficit, dizziness, tiredness, gait disturbance, falls, sarcopenia, bone fractures, osteoporosis, hypercalciuria (in the syndrome of inappropriate antidiuresis-SIADH), and kidney stones. In vitro studies have shown that cells grown in a low concentration of extracellular sodium have a greater proliferation rate and motility. Patients with chronic hyponatremia are more likely to develop cancer. We will not review the clinical consequences of respiratory arrest and osmotic demyelination syndrome (ODS) of the too-late or excessive treatment of hyponatremia.

Dysnatremias have been associated with an increased risk of mortality in the chronic kidney disease (CKD) population. Our objective is to identify the prevalence of and risk factors associated with dysnatremias in a CKD population and assess the association of dysnatremias with kidney failure and mortality among patients with CKD enrolled in the Chronic Renal Insufficiency Cohort Study.

Analysis of prospective cohort study.

Adult patients aged 21-74 years with CKD from the Chronic Renal Insufficiency Cohort study.

Baseline and time-dependent hyponatremia and hypernatremia.

All-cause mortality and kidney failure.

Baseline characteristics were compared using χ2 tests for categorical variables, analysis of variance for age, and Kruskal-Wallis tests for laboratory variables. Cox proportional hazards models and competing risk models were used to evaluate the association between baseline sodium level and overall mortality.

Of a total of 5,444 patients with CKD, 486 (9%) had hyponatremia and 53 (1%) had hypernatremia. Altogether, 1,508 patients died and 1,206 reached kidney failure. In adjusted Cox models, time-dependent dysnatremias were strongly associated with mortality for both hyponatremia (HR, 1.38; 95% CI, 1.16-1.64) and hypernatremia (HR, 1.54; 95% CI, 1.04-2.29). Factors associated with hyponatremia included female sex, diabetes, and hypertension. Regardless of age, time-dependent hypernatremia was associated with an increased risk of kidney failure (HR, 1.64; 95% CI, 1.06-2.53). Baseline and time-dependent hyponatremia were associated with an increased risk of kidney failure in patients younger than 65 (baseline hyponatremia HR, 1.30; 95% CI, 1.03-1.64 and time-dependent hyponatremia HR, 1.36; 95% CI, 1.09-1.70) but not among patients aged >65 years.

Inability to establish causality and lack of generalizability to hospitalized patients.

Dysnatremias are prevalent among ambulatory CKD patients and are associated with mortality and kidney failure. Time-dependent dysnatremias were significantly associated with mortality in patients with CKD. Time-dependent hypernatremia was associated with progression to kidney failure. Baseline and time-dependent hyponatremia were associated with an increased risk of progression to kidney failure in those younger than 65 years.

Hyponatremia is the most common electrolyte disturbance seen in clinical practice, affecting up to 30% of acute hospital admissions, and is associated with significant adverse clinical outcomes. Acute or severe symptomatic hyponatremia carries a high risk of neurological morbidity and mortality. In contrast, chronic hyponatremia is associated with significant morbidity including increased risk of falls, osteoporosis, fractures, gait instability, and cognitive decline; prolonged hospital admissions; and etiology-specific increase in mortality. In this Approach to the Patient, we review and compare the current recommendations, guidelines, and literature for diagnosis and treatment options for both acute and chronic hyponatremia, illustrated by 2 case studies. Particular focus is concentrated on the diagnosis and management of the syndrome of inappropriate antidiuresis. An understanding of the pathophysiology of hyponatremia, along with a synthesis of the duration of hyponatremia, biochemical severity, symptomatology, and blood volume status, forms the structure to guide the appropriate and timely management of hyponatremia. We present 2 illustrative cases that represent common presentations with hyponatremia and discuss the approach to management of these and other causes of hyponatremia.

Sodium abnormalities are frequent in central nervous system infections and may be caused by cerebral salt wasting, syndrome of inappropriate antidiuretic hormone secretion, or medication adverse events. In cryptococcal meningitis (CM), the prevalence of baseline hyponatremia and whether hyponatremia adversely impacts survival is unknown.

We conducted a secondary analysis of data from 2 randomized trials of human immunodeficiency virus-infected adult Ugandans with CM. We grouped serum sodium into 3 categories: <125, 125-129, and 130-145 mmol/L. We assessed whether baseline sodium abnormalities were associated with clinical characteristics and survival.

Of 816 participants with CM, 741 (91%) had a baseline sodium measurement available: 121 (16%) had grade 3-4 hyponatremia (<125 mmol/L), 194 (26%) had grade 2 hyponatremia (125-129 mmol/L), and 426 (57%) had a baseline sodium of 130-145 mmol/L. Hyponatremia (<125 mmol/L) was associated with higher initial cerebrospinal fluid (CSF) quantitative culture burden (P < .001), higher initial CSF opening pressure (P < .01), lower baseline Glasgow Coma Scale score (P < .01), and a higher percentage of baseline seizures (P = .03). Serum sodium <125 mmol/L was associated with increased 2-week mortality in unadjusted and adjusted survival analyses (adjusted hazard ratio, 1.87 [95% confidence interval, 1.26-2.79]; P < .01) compared to those with sodium 130-145 mmol/L.

Hyponatremia is common in CM and is associated with excess mortality. A standardized management approach to correctly diagnose and correct hyponatremia in CM needs to be developed and tested.

Hyponatremia and hypernatremia are common electrolyte abnormalities in patients with malignancy and have been independently associated with worse survival outcomes. To date, there are no data on the impact of dysnatremia on survival outcomes in patients with neuroendocrine neoplasms (NENs).

This study involves retrospective cohort analysis from a tertiary care center of NEN patients treated with peptide receptor radionuclide therapy (PRRT) with a cumulative activity of at least 3.7 GBq 177Lu-DOTATATE between the years 2000 and 2015.

Comparison of overall survival of patients with the occurrence of hyponatremia (serum sodium < 135 mmol/L) or hypernatremia (serum sodium > 145 mmol/L) before starting or during PRRT was perfomed.

A total of 649 patients were included. Hyponatremia occurred in 57 patients during the observation period and was associated with a shorter median overall survival (95% CI) of 25 months (14-36) compared to 55 months (48-61) of the 512 normonatremic patients (P < 0.001), adjusted hazard ratio (HR): 1.48 (95% CI: 1.04-2.12). Overall survival time was reduced regardless of whether hyponatremia was present at baseline or during PRRT. In contrast, hypernatremia occurred in 80 patients and was associated with a longer median overall survival (95% CI) of 94 months (47-140) compared with the 512 normonatremic patients (P = 0.018), adjusted HR: 0.61 (95% CI: 0.40-0.92). This association was driven by the patients with hypernatremia during PRRT. No association between dysnatremia and progression-free survival after PRRT was observed.

The occurrence of hypo- or hypernatremia in PRRT-treated NET patients is associated with opposing outcomes with regard to overall survival. Sodium levels might have a prognostic role in these patients.

Hyponatremia is a prognostic marker for specific pathologies. However, the association between contrast-induced nephropathy (CIN) and post-procedural hyponatremia has not been explored. Our study aims to evaluate the association between hyponatremia developing after contrast media administration and CIN.

A total number of 236 patients who required nephrology consultation before coronary angiography (CAG) or percutaneous coronary intervention (PCI) because of the high risk for contrast nephropathy, were included. Serum sodium levels were measured at admission and within three consecutive days after contrast media administration.

Hyponatremia was observed in 141patients (59.7%) following angiography. CIN was developed in 149 (63.4%) patients. Among the patients who developed hyponatremia, ejection fraction, serum haemoglobin level and serum albumin level were low whereas, contrast media volume and percentage of the diabetes mellitus were higher. Also, length of hospital stay, percentage of CIN, renal replacement requirement and mortality rate were higher in patients with hyponatremia. In univariable analysis to evaluate the risk factors for CIN, being female gender, age, diabetes mellitus, serum albumin concentration, haemoglobin level, contrast media volume and hyponatremia were associated with development of CIN. Multivariable logistic regression analysis revealed that advanced age, serum albumin concentration and hyponatremia were independent predictors of CIN.

Post-procedural hyponatremia was an independent risk factor for CIN in CAG or PCI patients.

This study was aimed at determining the risk factors associated with mortality in elderly patients with severe hyponatremia admitted to the emergency department.

The data of patients aged ≥ 65 years who were admitted to the emergency department and whose serum sodium levels were < 125 mEq/L were retrospectively collected.

Mortality was associated with chronic liver disease/cirrhosis (p = 0.036), metastatic tumor (p = 0.007) and solid tumor (p = 0.013) cancers, antiarrhythmic drug use (p = 0.003), potassium-sparing diuretic use (p = 0.044), antineoplastic drug use (p = 0.0029), and dialysis treatment (p = 0.015). The following cutoff values were determined to be predictive of mortality: urea > 63.6 (AUC: 0.771; p = 0.0001), creatinine > 1.39 (AUC: 0.675; p = 0.0003), potassium > 4.64 (AUC: 0.711; p = 0.0001), C-reactive protein > 44 (AUC: 0.765; p = 0.0001), white blood cell count > 12.21 (AUC: 0.688; p = 0.0001), hemoglobin < 11.2 (AUC: 0.611; p = 0.0103), and Charlson comorbidity index > 2 (AUC: 0.739; p = 0.0001). The use of antineoplastic drugs (OR: 4.502; p = 0.010) and increased values of the following were associated with an increased risk of mortality: urea (OR: 1.007; p = 0.024), C-reactive protein (OR: 1.005; p = 0.026), glucose (OR: 1.008; p = 0.001), and Charlson comorbidity index (OR: 1.198; p = 0.025).

Malignancy; liver cirrhosis; dialysis treatment; increased Charlson comorbidity index, urea, and C-reactive protein values and the use of antineoplastic drugs are associated with mortality.