In clinical medicine, the assessment of hyponatremia is frequently required but also known as a source of major diagnostic errors, substantial mismanagement, and iatrogenic morbidity. Because artificial intelligence techniques are efficient in analyzing complex problems, their use may possibly overcome current assessment limitations. There is no literature concerning Chat Generative Pre-trained Transformer (ChatGPT-3.5) use for evaluating difficult hyponatremia cases. Because of the interesting pathophysiology, hyponatremia cases are often used in medical education for students to evaluate patients with students increasingly using artificial intelligence as a diagnostic tool. To evaluate this possibility, four challenging hyponatremia cases published previously, were presented to the free ChatGPT-3.5 for diagnosis and treatment suggestions.

We used four challenging hyponatremia cases, that were evaluated by 46 physicians in Canada, the Netherlands, South-Africa, Taiwan, and USA, and published previously. These four cases were presented two times in the free ChatGPT, version 3.5 in December 2023 as well as in September 2024 with the request to recommend diagnosis and therapy. Responses by ChatGPT were compared with those of the clinicians.

Case 1 and 3 have a single cause of hyponatremia. Case 2 and 4 have two contributing hyponatremia features. Neither ChatGPT, in 2023, nor the previously published assessment by 46 clinicians, whose assessment was described in the original publication, recognized the most crucial cause of hyponatremia with major therapeutic consequences in all four cases. In 2024 ChatGPT properly diagnosed and suggested adequate management in one case. Concurrent Addison's disease was correctly recognized in case 1 by ChatGPT in 2023 and 2024, whereas 81% of the clinicians missed this diagnosis. No proper therapeutic recommendations were given by ChatGPT in 2023 in any of the four cases, but in one case adequate advice was given by ChatGPT in 2024. The 46 clinicians recommended inadequate therapy in 65%, 57%, 2%, and 76%, respectively in case 1 to 4.

Our study currently does not support the use of the free version ChatGPT 3.5 in difficult hyponatremia cases, but a small improvement was observed after ten months with the same ChatGPT 3.5 version. Patients, health professionals, medical educators and students should be aware of the shortcomings of diagnosis and therapy suggestions by ChatGPT.

Background and objectives: hyponatremia is a common in older and hospitalized patients, often caused by the syndrome of inappropriate antidiuretic hormone secretion (SIADH). This study compares the efficacy and safety of tolvaptan versus fluid restriction in patients with hyponatremia and SIADH. Materials and methods: an observational cohort study was conducted with 186 patients with hyponatremia (Na+ < 135 mmol/L) due to SIADH, treated at the Hospital Universitario de Pontevedra between 2015 and 2022. Of these, 86 were treated with tolvaptan (mean dose of 7.5 mg) and 100 with fluid restriction (1 liter of fluids per day). The primary endpoint was the normalization of sodium levels (Na ≥ 135 mmol/L). Results: tolvaptan was more effective than fluid restriction in correcting hyponatremia, increasing plasma sodium from 125.09 to 135.69 mmol/L in 4 days, compared to an increase from 126.44 to 130.5 mmol/L in 8 days with fluid restriction (p < 0.001). Mortality at 60 days was lower in the tolvaptan group (12.8 % vs. 32.8 %, p < 0.003). However, tolvaptan showed higher risks of sodium overcorrection (10.46 %) and polyuria (5.81 %), while fluid restriction was associated with greater dehydration, headache, and cramps. Conclusion: tolvaptan corrects hyponatremia more quickly and effectively than fluid restriction, although with a higher risk of overcorrection and polyuria, and is associated with lower 60-day mortality.

Three percent hypertonic saline (3NS) is an established treatment for severe hyponatremia. The optimal regimen for administering 3NS for severe hyponatremia, with the aim to minimize side effects is not known. This systematic review and meta-analysis aimed to evaluate the safety profile of rapid intermittent bolus (RIB) versus slow continuous infusion (SCI) of 3NS for managing symptomatic severe hyponatremia.

Databases were searched for studies evaluating the use of RIB versus SCI/conventional therapy of 3NS for managing symptomatic severe hyponatremia. The primary outcome was to evaluate the occurrence of overcorrection of hyponatremia. Secondary outcomes were to evaluate the need for relowering therapy, duration of hospital stay, changes in sodium levels, osmotic demyelination syndrome (ODS), and mortality.

Data from three studies (290 patients) with severe hyponatremia was analyzed. Patients receiving RIB had a similar occurrence of overcorrection (relative risk [RR]: 1.59 [0.40, 6.35]; I2 = 61%; P = 0.51), need for relowering treatment to bring down serum sodium back to the normal range (RR: 2.53 [0.32, 20.20]; I2 = 81%; P = 0.38), ODS (RR: 2.24 [0.09, 57.18]; P = 0.63) and mortality (RR: 0.51 [0.08, 3.30]; I2 = 31%; P = 0.48), as compared to those receiving SCI. Patients receiving RIB had a marginally higher duration of hospital stay, which approached statistical significance (mean difference: 3.71 days [-0.18, 7.59]; I2 = 0%; P = 0.06).

Both RIB and SCI of hypertonic saline were safe and effective for managing severe symptomatic hyponatremia. The reduced duration of hospital stay with SCI of hypertonic saline may suggest this may be the optimal way of administering hypertonic saline.

Objective Overly rapid correction of profound hyponatremia can lead to osmotic demyelination syndrome; however, the incidence of and risk factors for overly rapid correction in patients with profound hyponatremia have not been thoroughly examined. Therefore, this study examined the incidence of and risk factors for overly rapid correction in patients with profound hyponatremia. Methods This single-center, retrospective cohort study conducted at an 865-bed teaching hospital analyzed data from 144 new inpatients with profound hyponatremia [initial serum sodium (Na+) level of <125 mEq/L] treated in our department between January 2014 and December 2022. Overly rapid correction was defined as serum Na+ correction of >10 mEq/L at 24 h. We examined the incidence of and risk factors for overly rapid correction. Results Thirty (20.8%) patients met the overly rapid correction criteria; however, none developed osmotic demyelination syndrome. A low initial serum Na+ level, female sex, primary polydipsia, and low frequency of follow-up in 24 h were significant independent risk factors for overly rapid correction in the multivariable analysis (p=0.020, p=0.011, p=0.014, and p=0.025, respectively). Conclusion Our study shows that a low initial serum Na+ level, female sex, primary polydipsia, and low frequency of follow-up within 24 h are associated with an increased risk for overly rapid correction of profound hyponatremia. Therefore, we suggest that physicians perform careful management when managing patients with profound hyponatremia with the risk factors for overly rapid correction identified in this study.

Continuous venovenous hemofiltration (CVVH) is frequently performed in critically ill patients using diluted citrate for regional anticoagulation. The impact of this renal replacement strategy on plasma sodium has not been evaluated yet. Our aim was therefore to assess the period prevalence of hyponatremia (sodium <135 mmol/L) during CVVH and discuss possible underlying mechanisms. After 48 hours of treatment, 70% of the 27 oligo-anuric critically ill patients were hyponatremic, despite the use of dialysis fluid bags (Regiocit 18/0, Phoxilium by Baxter, Deerfield, IL, and Multibic K2 by Fresenius Medical Care AG & Co. KGaA, Bad Homburg, Germany) with sodium content of 140 mmol/L. Indeed, sodium decreased from 142 ± 7 to 135 ± 3 mmol/L, p < 0.001. Sodium concentrations of employed dialysis bags were confirmed using ion chromatography. However, ionized sodium of Regiocit measured with a direct-ion selective electrode (ISE) resulted lower (~118 mmol/L), suggesting the presence of sodium-to-citrate complexes. Possible mechanisms explaining the hyponatremia development could therefore include: i) plasma water dilution; ii) a reduced Gibbs-Donnan effect, given the low albumin concentration (2.6 ± 0.8 g/dl) of our critically ill patients; iii) a negative sodium balance due to the loss of sodium-to-citrate complexes across the filter. The clinical implications of the described hyponatremia and the different contributions of the hypothesized mechanisms need to be addressed in future studies.

Osmotic demyelination syndrome (ODS) is a rare but severe condition often attributed to the rate of sodium collection. We evaluated the association between the overly rapid sodium correction in adult hospitalized patients with ODS.

Systematic review and meta-analysis.

Adults hospitalized hyponatremia patients.

The studies comparing the incidence of ODS with and without rapid sodium correction inception to January 2024.

Two reviewers independently extracted data and assessed the risk of bias and the certainty of evidence.

The incidence of ODS following a rapid and nonrapid sodium correction was pooled using the random effects model. Subgroup and meta-regression analyses were performed for the robustness and the source of heterogeneity.

Eleven cohort studies were included with 26,710 hospitalized hyponatremia patients. The definition of hyponatremia varied from <116 to <130 mmol/L, and overly rapid sodium correction was defined as >8 to 12 mmol/L within 24 hours. The overall incidence of ODS was 0.23%. The incidence of ODS in rapid and nonrapid sodium correction was 0.73% and 0.10%, respectively. Meta-analysis demonstrated that a rapid rate of sodium correction was associated with a higher incidence of ODS (odds ratio 3.16, 95% CI, 1.54-6.49, I2 = 27%), whereas some patients with hyponatremia developed ODS without rapid sodium level correction. The sensitivity analysis based on the quality of the studies was consistent with the main result.

Various definition criteria for ODS diagnosis across studies, lack of potential electrolyte and treatment data that may affect the incidence of ODS.

The rapid rate of sodium correction had a statistical correlation with a higher incidence of ODS. Among ODS without rapid correction, further studies are recommended to evaluate and comprehend the relationship for better and proper management of hospitalized patients with hyponatremia.

In clinical medicine, hyponatremia is highly prevalent and frequently misdiagnosed, leading to substantial mismanagement and iatrogenic morbidity. Its differential diagnosis includes numerous diseases with diverse etiologies, making accurate assessment challenging. Despite extensive literature and guidelines on hyponatremia, most patients do not receive adequate evaluation due to the limitations of diagnostic algorithms, which rely on low-value clinical signs and are unable to identify concurrent conditions. In this review, we examine the range of laboratory tests available for hyponatremia assessment. Understanding renal mechanisms of solute and water exchange (e.g., fractional excretion) is essential for selecting appropriate tests and interpreting their diagnostic value. Additionally, detailed electrolyte and acid-base assessments remain critical for establishing a definitive diagnosis. We comprehensively discuss the selection of laboratory tests for specific differential diagnoses of hyponatremia. Importantly, in cases of acute hyponatremia, rapid correction should take precedence over a complete diagnostic workup. Ultimately, a thorough understanding of laboratory evaluation is crucial for accurately diagnosing hyponatremia. This paper critically reviews the available literature and explores relevant diseases in the context of associated laboratory parameters.

Oral urea is being used more commonly to treat hyponatremia, but factors contributing to the correction rate are unknown. We hypothesized that clinically relevant factors can be identified to help guide hyponatremia correction with oral urea.

This was a retrospective study in two university hospitals including hospitalized patients with hyponatremia (plasma sodium <135 mmol/L) treated with oral urea. Linear mixed-effects models were used to identify factors associated with hyponatremia correction. Rates of overcorrection, osmotic demyelination and treatment discontinuation were also assessed.

We included 161 urea treatment episodes in 140 patients (median age 69 years, 46% females, 93% syndrome of inappropriate antidiuresis). Oral urea succeeded fluid restriction in 117 treatment episodes (73%), was combined with fluid restriction in 104 treatment episodes (65%) and was given as the only treatment in 27 treatment episodes (17%). A median dose of 30 g/day of urea for 4 days (interquartile range 2-7 days) increased plasma sodium from 127 to 134 mmol/L and normalized hyponatremia in 47% of treatment episodes. Older age (β 0.09, 95% CI 0.02-0.16), lower baseline plasma sodium (β -0.65, 95% CI -0.78 to -0.62) and higher cumulative urea dose (β 0.03, 95% CI -0.02 to -0.03) were independently associated with a greater rise in plasma sodium. Concurrent fluid restriction was associated with a greater rise in plasma sodium only during the first 48 h of treatment (β 1.81, 95% CI 0.40-3.08). Overcorrection occurred in 5 cases (3%), no cases of osmotic demyelination were identified and oral urea was discontinued in 11 cases (11%) due to side effects.

During treatment with oral urea, older age, higher cumulative dose, lower baseline plasma sodium and initial fluid restriction are associated with a greater correction rate of hyponatremia. These factors may guide clinicians to achieve a gradual correction of hyponatremia with oral urea.

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.

Mesoamerican nephropathy (MeN) is a progressive kidney disease found on the Pacific coast of Central America primarily in young male agricultural workers without typical kidney disease risk factors. While it is generally accepted that environmental exposures contribute to MeN, we hypothesized that there was also an important genetic component. We performed a genome-wide association study comparing individuals with MeN versus individuals with normal kidney function. We found that Native American ancestry was strongly associated with increased risk of MeN. We also identified candidate variants in the OPCML gene, which encodes a protein that binds opioid receptors, that were associated with ~sixfold reduced odds of MeN (allele frequency 0.029 in controls and 0.005 in cases, OR = 0.16; P = 4 × 10-8). Sugarcane workers with the protective OPCML variants had markedly increased urine osmolality suggesting greater ability to defend against hypovolemia. Experiments with Opcml knock-out mice revealed roles for OPCML in fluid balance and temperature regulation consistent with our findings in humans. Our data suggest that heritable differential sensitivity to heat stress and dehydration contributes to high rates of kidney disease in Central America.

Patients undergoing solid-organ transplantation (SOT) face a tumultuous journey. Prior to transplant, their medical course is characterized by organ dysfunction, diminished quality of life, and reliance on organ support, all of which are endured in hopes of reaching the haven of organ transplantation. Peritransplant altered mental status may indicate neurologic insults acquired during transplant and may have long-lasting consequences. Even years after transplant, these patients are at heightened risk for neurologic dysfunction from a myriad of metabolic, toxic, and infectious causes. This review provides a comprehensive examination of causes, diagnostic approaches, neuroimaging findings, and management strategies for altered mental status in SOT recipients. Given their complexity and the numerous etiologies for neurologic dysfunction, liver transplant patients are a chief focus in this review; however, we also review lesser-known contributors to neurological injury across various transplant types. From hepatic encephalopathy to cerebral edema, seizures, and infections, this review highlights the importance of recognizing and managing pre- and posttransplant neurological complications to optimize patient outcomes.

Hyponatraemia is the most common electrolyte disorder in hospital patients associated with increased morbidity, mortality, hospital stay and financial burden. The speed of a correction with 3% sodium chloride as a 100- to 150-ml intravenous bolus or continuous infusion depends on the severity and persistence of the symptoms and needs frequent biochemical monitoring. The rapid intermittent administration of hypertonic saline is preferred for treatment of symptomatic hyponatraemia. In asymptomatic mild hyponatraemia, an adequate solute intake with an initial fluid restriction (FR) of 500 ml/day adjusted according to the serum sodium (sNa) levels is preferred. Almost half of the syndrome of inappropriate antidiuretic hormone (SIADH) patients do not respond to FR as first-line therapy. At present, urea and tolvaptan are considered the most effective second-line therapies in SIADH. However, the evidence for guidance on the choice of second-line therapy of hypotonic hyponatraemia is lacking. Oral urea is considered to be a very effective and safe treatment. Mild and asymptomatic hyponatraemia is treated with adequate solute intake (salt and protein) and initial FR with adjustments based on sNa levels. Specific treatment with vaptans may be considered in either euvolaemic or hypervolaemic patients with high ADH activity. In order to ensure optimal patient outcome, close monitoring and readiness for administration of either hypotonic fluids or desmopressin may be crucial in the decision-making process for specific treatment and eventual overcorrection consequences. According to the guidelines, gradual correction and clinical evaluation is preferable over rapid normalization of sNa towards the laboratory reference ranges.

Benzodiazepines (BZDs) are among the most commonly used medications due to their efficacy and rapid onset of action. Although they offer significant therapeutic benefits in treating various psychiatric and neurological conditions, their clinical utility is limited by substantial risks, including dependency and withdrawal symptoms. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) has been linked to BZD withdrawal. In this case report, we examine the case of an elderly female presented with a mixed delirium and SIADH following the abrupt cessation of long-term clonazepam therapy. To our knowledge, this is the second case that documents a link between SIADH and BZD withdrawal.

Background and Subject: Hyponatraemia is a common electrolyte disorder. For patients with severe hyponatraemia, intensive care unit (ICU) admission may be required. This will enable close monitoring and allow safe management of sodium levels effectively. While severe hyponatraemia may be associated with significant symptoms, rapid overcorrection of hyponatraemia can lead to complications. We aimed to describe the management and outcomes of severe hyponatraemia in our ICU and identify risk factors for overcorrection. Materials and Methods: This was a retrospective single-centre cohort that included consecutive adults admitted to the ICU with serum sodium < 120 mmol/L between 1 January 2017 and 8 March 2023. Anonymised data were collected from electronic records. We included 181 patients (median age 67 years, 51% male). Results: Median admission serum sodium was 113 mmol/L (IQR: 108-117), with an average rate of improvement over the first 48 h of 10 mmol/L/day (IQR: 5-15 mmol/L). A total of 62 patients (34%) met the criteria for overcorrection at 48 h, and they were younger, presented with severe symptoms (seizures/arrythmias), and had lower admission sodium concentration. They were more likely to be treated with hypertonic saline infusions. Lower admission sodium was an independent risk factor for overcorrection within 48 h, whereas the presence of liver cirrhosis and fluid restriction was associated with normal correction. No difference was identified between the normal and overcorrected cohorts for ICU/hospital length of stay or mortality. Conclusions: In some patients with severe hyponatraemia, overcorrection is inevitable to avoid symptoms such as seizures and arrhythmias, and consequently, we highlight the key factors associated with overcorrection. Overall, we identified that overcorrection was common and concordant with the current literature.

Aim The aim of this study is to analyze the demographic distribution (age and gender distribution), presenting symptoms, and evaluate the underlying etiology of hyponatremia among the study population. The presence of comorbidities and the volume status (hypovolemia, euvolemia, or hypervolemia) of elderly hyponatremic patients with varying severity of hyponatremia were assessed. Methods This cross-sectional, observational study was conducted in Dr. D. Y. Patil Hospital and Research Centre, Pune, India. After approval from the Institutional Ethics Sub-Committee (approval number: IESC/PGS/2022/09), it was conducted during the period between September 2022 and June 2024. The minimum sample size was calculated to be 96 with a confidence interval of 95% using WINIPEPI software (version 11.38). The lab values of serum sodium of all patients aged above 60 years admitted in wards and intensive care units (ICUs) were studied. Out of these hyponatremic patients, a sample size of 100 patients was randomly selected. Patients above 60 years and the patients who were on diuretic therapy were excluded from the study. Results The study included 100 elderly patients with a mean age of 73.25 ± 7.03 years, ranging from 64 to 86 years. Males predominated (63%), and severe hyponatremia (<125 mEq/L) was the most common, affecting 61% of patients. Generalized weakness (22%) and disorientation (17%) were the most frequently reported symptoms. Post-operative conditions (13%) and gastroenteritis (10%) were the leading causes. Most participants had no comorbidities (53%). Hypovolemia was present in 67% and euvolemia in 29% of the study subjects. Among hypovolemic patients, severe hyponatremia was present in 83.5% of patients. Conclusion This study highlights the significant burden of severe hyponatremia among elderly patients, particularly in male subjects and those with hypovolemia. Majority of the participants did not have any comorbidities. Additionally, the study emphasizes the need for heightened clinical vigilance in elderly patients presenting with generalized weakness and disorientation, as these were the most common symptoms associated with hyponatremia. The identification of post-operative conditions and gastroenteritis as leading causes further supports the need for comprehensive management strategies in elderly inpatients to prevent the occurrence and complications of hyponatremia.

Animal models of a variety of acquired nephrogenic diabetes insipidus (NDI) disorders have identified a common feature: all such models are associated with the loss of aquaporin-2 (AQP2) from collecting duct principal cells, explaining the associated polyuria. To discover mechanisms of AQP2 loss, previous investigators have carried out either transcriptomics (lithium-induced NDI, unilateral ureteral obstruction, endotoxin-induced NDI) or proteomics (hypokalaemia-associated NDI, hypercalcaemia-associated NDI, bilateral ureteral obstruction), yielding contrasting views. Here, to address whether there may be common mechanisms underlying loss of AQP2 in acquired NDI disorders, we have used bioinformatic data integration techniques to combine information from all transcriptomic and proteomic data sets. The analysis reveals roles for autophagy/apoptosis, oxidative stress and inflammatory signalling as key elements of the mechanism that results in loss of AQP2. These processes can cause AQP2 loss through the combined effects of repression of Aqp2 gene transcription, generalized translational repression, and increased autophagic degradation of proteins including AQP2. Two possible types of stress-sensor proteins, namely death receptors and stress-sensitive protein kinases of the EIF2AK family, are discussed as potential triggers for signalling processes that result in loss of AQP2. KEY POINTS: Prior studies have shown in a variety of animal models of acquired nephrogenic diabetes insipidus (NDI) that loss of the aquaporin-2 (AQP2) protein is a common feature. Investigations of acquired NDI using transcriptomics (RNA-seq) and proteomics (protein mass spectrometry) have led to differing conclusions regarding mechanisms of AQP2 loss. Bioinformatic integration of transcriptomic and proteomic data from these prior studies now reveals that acquired NDI models map to three core processes: oxidative stress, apoptosis/autophagy and inflammatory signalling. These processes cause loss of AQP2 through translational repression, accelerated degradation of proteins, and transcriptional repression.

To describe the feasibility of managing hyponatremia patients under outpatient observation status in an academic medical center, and compare outcomes based on the use of an emergency department observation unit (EDOU).

This is a retrospective cohort study of emergency department hyponatremic patients managed in four hospitals within a large urban academic medical center over 27 months. All patients had an admit-to-observation order, ICD-10 codes for hyponatremia, and mild (130-135 mmol/L) to moderate (121-129 mmol/L) hyponatremia. Observation settings were divided into two groups: EDOU and Non-Observation Unit (NOU) inpatient beds. Severe hyponatremia (≤120 mmol/L) was excluded. Primary clinical outcomes were inpatient admit rate, length of stay (LOS), total direct cost, the rate of adverse events and 30-day recidivism.

188 patients were managed as an observation patient, with 64 managed in an EDOU setting (age 74.0 yr, 70.3% female) and 124 managed in a NOU setting (age 71.5 yr, 64.5% female). Patient subgroups were similar in terms of presenting complaints, comorbidities, and medication histories. Initial and final sodium levels were similar between settings: EDOU (125.1 to 132.6 mmol/L) vs NOU (123.5 to 132.0 mmol/L). However, outcomes differed by setting for observation to inpatient admit rate (EDOU 28.1% vs NOU 37.9%, adjusted effect 0.70), overall length of stay (EDOU 19.2 h vs NOU 31.9 h; adjusted effect -10.5 h and total direct cost ($1230 vs $1531; adjusted effect -$167). EDOU sodium correction rates were faster (EDOU 0.44 mmol/L/h vs 0.24 mmol/L/h; adjusted effect 0.15 mmol/L/h) and 30-day recidivism rate was similar (EDOU 13% vs NOU 15%). There were no index visit deaths or intensive care unit admissions.

Management of selected hyponatremia patients under observation status is feasible, with the EDOU setting demonstrating lower admit rates, shorter length of stay, and lower total direct costs with similar clinical outcomes.

To determine the factors affecting mortality as a result of the analysis of the demographic and clinical characteristics and laboratory parameters of patients whose serum Na value was determined to be 125 mEq/L or below at the time of admission to the emergency department (ED).

Patients over 18 years of age who admitted to the ED of a tertiary hospital between September 2021 and September 2022 and whose serum sodium level was determined to be 125 mEq/L and below were included in the study. Demographic and clinical characteristics, admission complaints, medications used, Charles comorbidity index (CCI), laboratory parameters, and outcomes of the patients included in the study were recorded in the data form.

Three hundred ninety-nine patients were included in the study. When the 30-day mortality of the patients is examined, the mortality rate was found to be 21.6%. In the analyses performed for the predictive power of laboratory parameters for mortality, it was determined that the highest predictive power among the predictive values determined by the area under the curve (AUC) was the albumin level (AUC 0.801, 95% CI 0.753-0.849, p < 0.001). In the binary logistic regression analysis, urea and albumin were independent predictors of 30-day mortality.

According to study data, albumin and urea levels are independent predictors of 30-day mortality in patients diagnosed with severe hyponatremia in the emergency department.

Clinical hyponatremia guidelines, protocols and flowcharts are a convenient means for clinicians to quickly establish an etiological diagnosis for hyponatremia, and facilitate its often complex analysis. Unfortunately, they often erroneously attribute multifactorial hyponatremia to a single cause, which is potentially dangerous. In this manuscript, a novel criterion is proposed to quickly determine the physiological relevance of non-osmotic arginine vasopressin (AVP) release, and to add nuance to hyponatremia analysis. While analyzing hypotonic hyponatremia, it is imperative to not only verify whether or not a certain degree of inappropriate AVP release is present, but also to ascertain whether it-in itself-could sufficiently explain the observed hyponatremia, as these two are not always synonymous. Using well-known concepts from renal physiology to combine the electrolyte-free water balance and solute-free water balance, a novel physiological criterion is derived mathematically to easily distinguish three common hyponatremia scenarios, and to further elucidate the underlying etiology. The derived criterion can hopefully facilitate the clinician's and physiologist's interpretation of plasma and urine parameters in a patient presenting with hyponatremia, and warn against the important clinical pitfall of attributing hyponatremia too readily to a single cause.

Hyponatremia is an adverse effect of many antiseizure medications (ASMs). It occurs with interference with the normal balance of electrolytes within the body. Various risk factors associated with the development of hyponatremia in patients taking these medications include age, gender, dosage, and combinations with other drugs. ASMs such as carbamazepine (CBZ), oxcarbazepine (OXC), and valproic acid have a higher risk of hyponatremia. Hyponatremia induced by an antiseizure medication can occur through various mechanisms depending on the drug's specific mechanism of action. Hyponatremia can be a potentially fatal side effect. Patients taking these medications need to be monitored closely for the signs and symptoms of hyponatremia. Acute hyponatremia, defined as developing in <48 hours, is more likely to show symptoms than chronic hyponatremia. Signs of acute hyponatremia include delirium, seizures, decerebrate posturing, and cerebral edema with uncal herniation. Chronic hyponatremia, defined as developing in >48 hours, can cause lethargy, dizziness, weakness, headache, nausea, and confusion. Hyponatremia is associated with longer hospital stays and increased mortality. Treatment varies based on the degree of severity of hyponatremia. Choosing a treatment option should include consideration of the drug causing the electrolyte disturbance, the patient's risk factor profile, and the severity of symptoms as they present in the individual patient. Healthcare providers should be aware of hyponatremia as a potential side effect of ASMs, the signs and symptoms of hyponatremia, the different treatment options available, and the potential complications associated with rapid correction of hyponatremia.

This randomized controlled trial aimed to evaluate the safety and efficacy of proactive versus reactive desmopressin (DDAVP) strategies in treating severe symptomatic hyponatremia. Conducted from June 20, 2022, to February 20, 2023, it involved 49 patients with serum sodium levels below 125 mmol/L. Patients were assigned to either the proactive group, receiving DDAVP immediately upon diagnosis, or the reactive group, receiving DDAVP only if the serum sodium level tended to be overcorrected. The primary outcome was the incidence of overcorrection. The study revealed no significant difference in the overcorrection incidence between the proactive (16.7%) and reactive (28%) groups (p = 0.54). The change in serum sodium levels at 1, 6, 12, and 24 h were not different, however, at 48 h, the proactive group exhibited a higher but still safe change in serum sodium levels compared to the reactive group (10.3 ± 3.6 mmol/L vs. 7.7 ± 3.6 mmol/L, p = 0.013). Other parameters including time to symptom improvement, total intravenous fluid administered, DDAVP dose, urine volume, hospital stay duration, osmotic demyelination syndrome incidence, and 28-day mortality did not significantly differ between the groups. In conclusion, our findings suggest that there was no significant disparity in overcorrection rates between proactive and reactive DDAVP strategies for treating severe symptomatic hyponatremia. However, further large-scale studies are warranted to validate these results.

Hereditary spherocytosis/elliptocytosis is a non-immune hemolytic anemia caused by an alteration in the erythrocyte membrane that predisposes the cell to its lysis. This report presents a case of a 42-year-old woman with a history of spontaneous abortion, associated with postpartum bleeding, chronic anemia, and premature menopause. After five years, she consulted due to alterations in the state of consciousness and severe symptomatic hyponatremia, with a diagnosis of hypopituitarism, explained by a late Sheehan syndrome. During hospitalization, she developed non-immune hemolytic anemia associated with a positive osmotic fragility test. A diagnosis of hereditary spherocytosis/elliptocytosis was made. We correlate blood hypoosmolarity as a trigger with the in vitro hypotonic solution of the osmotic fragility test for the diagnosis of this disease. This association is not reported in the literature; in our case, we show the concomitant improvement of anemia with the increase in sodium levels and hormonal replacement.

Osmotic gradients over cell membranes lead to water movement into or out of cells. An intact osmoregulation prevents osmotic gradients, thereby protecting cells from swelling or shrinking. Na+ is the major cation in the extracellular fluid (ECF) and the major determinant of the osmolarity in the ECF, including plasma. Therefore, the plasma-Na+ concentration needs to be tightly regulated. An excess of electrolyte-free water decreases the concentration of osmolytes leading to hyponatremia. In contrast, a free water deficit increases the osmolyte concentration leading to hypernatremia. Pathophysiology-oriented approaches to dysnatremic patients help both clinicians and patients. Therapeutic interventions depend on the differentiation between acute and chronic, asymptomatic, and symptomatic dysnatremia, and on the patient's extracellular volume status. The therapeutic armamentarium for hyponatremia consists of water restriction, hypertonic infusions, urea, V2 receptor-blockers, and sodium-glucose cotransporter 2 (SGLT2) inhibitors. Patients with hypernatremia are treated with electrolyte-free water or hypotonic sodium-containing solutions depending on their volume status. Basic concepts in the management of dysnatremic patients are discussed.

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.

Postoperative dysnatremias, characterized by imbalances in serum sodium levels, have been linked to increased resource utilization and mortality in surgical and intensive care patients. The management of dysnatremias may involve medical interventions based on changes in sodium levels. In this study, we aimed to investigate the impact of postoperative changes in natremia on outcomes specifically in patients undergoing craniotomy.We conducted a retrospective analysis of patient records from the Department of Neurosurgery at West China Hospital, Sichuan University, covering the period from January 2011 to March 2021. We compared the highest and lowest sodium values in the first 14 postoperative days with the baseline values to define four categories for analysis: no change < 5 mmol/L; decrease > 5 mmol/L; increase > 5 mmol/L; both increase and decrease > 5 mmol/L. The primary outcome measure was 30-day mortality.A total of 12,713 patients were included in the study, and the overall postoperative mortality rate at 30 days was 2.1% (264 patients). The increase in sodium levels carried a particularly high risk, with a tenfold increase (OR 10.21; 95% CI 7.25-14.39) compared to patients with minimal or no change. Decreases in sodium levels were associated with an increase in mortality (OR 1.60; 95% CI 1.11-2.23).Moreover, the study revealed that postoperative sodium decrease was correlated with various complications, such as deep venous thrombosis, pneumonia, intracranial infection, urinary infection, seizures, myocardial infarction, and prolonged hospital length of stay. On the other hand, postoperative sodium increases were associated with acute kidney injury, deep venous thrombosis, pneumonia, intracranial infection, urinary infection, surgical site infection, seizures, myocardial infarction, and prolonged hospital length of stay.Changes in postoperative sodium levels were associated with increased complications, prolonged length of hospital stay, and 30-day mortality. Moreover, the severity of sodium change values correlated with higher mortality rates.

Syndrome of inappropriate antidiuresis (SIAD) is one of the most frequent causes of euvolemic hyponatremia (serum sodium levels < 135 mEq/L) and it represents more than 35% of hyponatremia cases in hospitalized patients. It is characterized by an inappropriate vasopressin (AVP)/antidiuretic hormone (ADH) secretion, which occurs independently from effective serum osmolality or circulating volume, leading to water retention via its action on type 2 vasopressin receptor in the distal renal tubules. Corpus callosum agenesis (CCA) is one of the most common congenital brain defects, which can be associated to alterations in serum sodium levels. This report presents a rare case of chronic hyponatremia associated with SIAD in a woman with CCA, whose correction of serum sodium levels only occurred following twice-daily tolvaptan administration.

A 30-year-old female was admitted to our hospital for non-acute hyponatremia with dizziness, headache, distal tremors, and concentration deficits. She had profound hyponatremia (Na 121 mmol/L) with measured plasma hypo-osmolality (259 mOsm/Kg) and urinary osmolality greater than 100 mOsm/Kg (517 mOsm/Kg). She presented clinically as normovolemic. After the exclusion of other causes of normovolemic hyponatremia, such as hypothyroidism and adrenal insufficiency, a diagnosis of SIAD was established. We have ruled out paraneoplastic, inflammatory, and infectious causes, as well as ischemic events. Her medical history showed a CCA and frontal teratoma. We administered tolvaptan initially at a low dosage (15 mg once a day) with persistence of hyponatremia. Therefore, the dosage was first doubled (30 mg once a day) and then increased to 45 mg once a day with an initial improvement in serum sodium levels, although not long-lasting. We therefore tried dividing the 45 mg tolvaptan administration into two doses of 30 mg and 15 mg respectively, using an off-label treatment schedule, thus achieving long-lasting serum sodium levels in the low-normal range associated with a general clinical improvement.

This report underlines the importance of the correct diagnosis, management and treatment of SIAD, as well as the need for further studies about the pharmacokinetics and pharmacodynamics of vasopressin receptor antagonists.

Tolvaptan, a vasopressin antagonist selective for the V2-subtype vasopressin receptor (V2R), is widely used in the treatment of hyponatremia and autosomal-dominant polycystic kidney disease (ADPKD). Its effects on signaling in collecting duct cells have not been fully characterized. Here, we perform RNA-seq in a collecting duct cell line (mpkCCD). The data show that tolvaptan inhibits the expression of mRNAs that were previously shown to be increased in response to vasopressin including aquaporin-2, but also reveals mRNA changes that were not readily predictable and suggest off-target actions of tolvaptan. One such action is activation of the MAPK kinase (ERK1/ERK2) pathway. Prior studies have shown that ERK1/ERK2 activation is essential in the regulation of a variety of cellular and physiological processes and can be associated with cell proliferation. In immunoblotting experiments, we demonstrated that ERK1/ERK2 phosphorylation in mpkCCD cells was significantly reduced by vasopressin, in contrast to the increases seen in non-collecting-duct cells overexpressing V2R in prior studies. We also found that tolvaptan has a strong effect to increase ERK1/ERK2 phosphorylation in the presence of vasopressin and that tolvaptan's effect to increase ERK1/ERK2 phosphorylation is absent in mpkCCD cells in which both protein kinase A (PKA)-catalytic subunits have been deleted. Thus, it appears that the tolvaptan effect to increase ERK activation is PKA-dependent and is not due to an off-target effect of tolvaptan. We conclude that in cells expressing V2R at endogenous levels: 1) vasopressin decreases ERK1/ERK2 activation; 2) in the presence of vasopressin, tolvaptan increases ERK1/ERK2 activation; and 3) these effects are PKA-dependent.NEW & NOTEWORTHY Vasopressin is a key hormone that regulates the function of the collecting duct of the kidney. ERK1 and ERK2 are enzymes that play key roles in physiological regulation in all cells. The authors used collecting duct cell cultures to investigate the effects of vasopressin and the vasopressin receptor antagonist tolvaptan on ERK1 and ERK2 phosphorylation and activation.

Hyponatremia is a common electrolyte abnormality with important prognostic and therapeutic implications. It might exert detrimental effects on various organ systems including the central nervous system (CNS), bone, and heart along with its potential association with poor quality of life. These adverse effects might be largely mediated through a variety of mechanisms including osmotic stress, dysfunctional transmembrane exchangers, and enhanced oxidative stress.Interestingly, hyponatremia might also have an important association with takotsubo syndrome (TTS) that has been universally considered as a reversible form of cardiomyopathy usually emerging in response to various stressors. In this context, severe hyponatremia was previously reported to serve as a direct trigger of TTS evolution largely through its potential impact on CNS and heart. However, pathogenetic and clinical implications of hyponatremia still need to be thoroughly evaluated in patients with TTS. This paper aims to analyze the clinical features of published cases with TTS primarily triggered by hyponatremia and also aims to discuss the association between hyponatremia and TTS from a broader perspective.

International guidelines designed to minimize the risk of complications that can occur when correcting severe hyponatremia have been widely accepted for a decade. On the basis of the results of a recent large retrospective study of patients hospitalized with hyponatremia, it has been suggested that hyponatremia guidelines have gone too far in limiting the rate of rise of the serum sodium concentration; the need for therapeutic caution and frequent monitoring of the serum sodium concentration has been questioned. These assertions are reminiscent of a controversy that began many years ago. After reviewing the history of that controversy, the evidence supporting the guidelines, and the validity of data challenging them, we conclude that current safeguards should not be abandoned. To do so would be akin to discarding your umbrella because you remained dry in a rainstorm. The authors of this review, who represent 20 medical centers in nine countries, have all contributed significantly to the literature on the subject. We urge clinicians to continue to treat severe hyponatremia cautiously and to wait for better evidence before adopting less stringent therapeutic limits.

Heart failure (HF) is a global health challenge. The perturbations in fluid and electrolyte equilibrium, particularly the compromised sodium balance associated with HF lead to high mortality rates. Hence, elucidating the correlation between serum sodium levels and the prognosis of HF is of paramount importance. This study aimed to conduct a comprehensive meta-analysis to thoroughly investigate the interplay between hyponatremia and the prognostic outlook of individuals with HF.

A comprehensive search of bibliographic databases including PubMed, Embase, and the Cochrane Central Register of Controlled Trials was conducted to identify relevant observational studies examining the association between hyponatremia and prognosis of HF. Data extraction, synthesis, and assessment of risk of bias were conducted. Meta-analytic methods, sensitivity analyses, and heterogeneity test were employed as appropriate to synthesize the data.

A total of 43,316 patients with HF were included spanning 25 selected studies. The pooled data revealed a notable association between hyponatremia and elevated risks across short and long-term mortality of HF. Specifically, hyponatremia was found to significantly increase the likelihood of all-cause mortality (Hazard ratio [HR] = 1.94, 95% confidence interval [CI]: 1.78-2.12); 1-year mortality (HR = 1.67, 95%CI: 1.46-1.90); 30-day mortality (HR = 2.03, 95%CI: 1.73-2.25); cardiac mortality (HR = 2.11, 95%CI: 1.81-2.46); and in-hospital mortality (HR = 1.64, 95%CI: 1.15-2.34).

Our meta-analysis emphasizes the significant impact of hyponatremia on mortality in the HF patient population, highlighting the critical importance of maintaining stable serum sodium levels in HF management.

We aimed to investigate the frequency of dysnatremia among patients admitted with COVID-19 infection and its association with inpatient mortality.

This retrospective longitudinal study was conducted for 12 weeks. Serum sodium levels were recorded at admission, during the hospital stay, and within 48 hours of discharge or death. Logistic regression was used to determine the predictors of mortality.

This study included 574 patients (69.7% men, age 55.6 ± 14.4 years). On admission, mean sodium was 135.9 ± 6.4 mEq/L; 39% had hyponatremia and 4.7% had hypernatremia. During admission, hypernatremia increased to 18.8%; maximum sodium in patients who survived was 140.6 ± 5.0 mEq/L versus 151.0 ± 9.9 mEq/L in those who died. The final sodium was 145.4 ± 9.4 mEq/L in patients who died versus 137.7 ± 3.7 mEq/L in those who survived (odds ratio [OR]: 1.22, 95% confidence interval [CI]: 1.13-1.32). Other predictors of mortality included ischemic heart disease (OR: 3.65, 95% CI: 1.39-9.61), acute kidney injury (OR: 6.07, 95% CI: 2.39-15.42), invasive ventilation (OR: 28.4, 95% CI: 11.14-72.40), and length of stay (OR: 0.91, 95% CI: 0.86-0.97).

Hypernatremia was frequently observed in patients who were critically ill and died and may be considered a predictor of mortality in COVID-19 infection.

Tolvaptan, a selective vasopressin V2-receptor antagonist, is approved for the treatment of SIADH-related hyponatremia, but its use is limited. The starting dose is usually 15 mg/day, but recent clinical experience suggests a lower starting dose (<15 mg/day) to reduce the risk of sodium overcorrection. However, long-term low-dose efficacy and safety has not been explored, so far. Aim of our study is to characterize safety and efficacy of long-term SIADH treatment with low-dose Tolvaptan.

We retrospectively evaluated 11 patients receiving low-dose Tolvaptan (<15 mg/day) for chronic SIADH due to neurological, idiopathic and neoplastic causes. Plasma sodium levels were measured before and 1, 3, 5, 15 and 30 days after starting Tolvaptan and then at 3-month intervals. Anamnestic and clinical data were collected.

Mean time spanned 27.3 ± 29.8 months (range 6 months-7 years). Mean plasma sodium levels were within normal range 1, 3 and 6 months after starting Tolvaptan as well as after 1, 2, 3, 5 and 7 years of therapy. Neither osmotic demyelination syndrome nor overcorrection were observed. Plasma sodium levels normalization was associated with beneficial clinical effects. Neurological patients obtained seizures disappearance, improvement in neurological picture and good recovery from rehabilitation. Neoplastic patients were able to start chemotherapy and improved their general condition. Patients did not show hypernatremia during long-term follow-up and reported mild thirst and pollakiuria.

The present study shows that long-term low-dose Tolvaptan is safe and effective in SIADH treatment. No cases of overcorrection were documented and mild side effects were reported.

Sodium imbalances are a common occurrence in the emergency department. Although recognition and diagnosis are relatively straightforward, discovering the cause and management should be approached systematically. The most important history items to ascertain is if the patient has symptoms and how long this imbalance has taken to develop. Treatment rapidity depends on severity of symptoms with the most rapid treatment occurring in only the severely symptomatic. Overcorrection has dire consequences and must be approached in a careful and systematic fashion in order to prevent these devastating consequences.

Hyponatraemia on hospital admission is associated with increased length of stay, healthcare expenditures and mortality. Urine studies collected before fluid or diuretic administration are essential to diagnose the underlying cause of hyponatraemia, thereby empowering admitting teams to employ the appropriate treatment. A multidisciplinary quality improvement (QI) team led by internal medicine residents performed a QI project from July 2020 through June 2021 to increase the rate of urine studies collected before fluid or diuretic administration in the emergency department (ED) in patients admitted with moderate to severe hyponatraemia. We implemented two plan-do-study-act (PDSA) cycles to address this goal. In PDSA Cycle #1, we displayed an educational poster in employee areas of the ED and met with nursing staff at their monthly meetings to communicate the project and answer questions. We also obtained agreement from ED attending physicians and nursing leaders to support the project. In PDSA Cycle #2, we implemented a structural change in the nursing triage process to issue every patient who qualified for bloodwork with a urine specimen container labelled with a medical record number on registration so that the patient could provide a sample at any point, including while in the waiting area. After PDSA Cycle #1, urine specimen collection increased from 34.5% to 57.5%. After PDSA Cycle #2, this increased further to 59%. We conclude that a combination of educational and structural changes led to a significant increase in urine specimen collection before fluid or diuretic administration among patients presenting with moderate-to-severe hyponatraemia in the ED.

Stroke mimics typically involve non-vascular disease processes, accounting for approximately half of hospital admissions for suspected stroke. These mimics may manifest as functional (conversion) disorders or indicate other neurological or medical conditions, including hypoglycemia, brain tumors, toxic poisoning, migraines, sepsis, seizures, and electrolyte imbalances, which can imitate stroke symptoms, making the diagnosis complex. In this report, we present a unique case of a man in his sixties who developed acute postoperative hyponatremia, an electrolyte abnormality frequently encountered but rarely presented with focal neurological deficits. This condition resulted in facial asymmetry and hemiparesis; however, the remarkable outcome was that these deficits were completely resolved once the hyponatremia was corrected.

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.

Differential diagnosis of thiazide-associated hyponatremia (TAH) is challenging. Patients can either have volume depletion or a syndrome of inappropriate antidiuresis (SIAD)-like presentation.

To evaluate the impact of the simplified apparent strong ion difference in serum (aSID; sodium + potassium - chloride) as well as the urine chloride and potassium score (ChU; chloride - potassium in urine) in the differential diagnosis of TAH, in addition to assessment of fractional uric acid excretion (FUA).

Post hoc analysis of prospectively collected data from June 2011 to August 2013 from 98 hospitalized patients with TAH < 125 mmol/L enrolled at University Hospital Basel and University Medical Clinic Aarau, Switzerland. Patients were categorized according to treatment response in volume-depleted TAH requiring volume substitution or SIAD-like TAH requiring fluid restriction. We computed sensitivity analyses with ROC curves for positive predictive value (PPV) and negative predictive value (NPV) of aSID, ChU, and FUA in differential diagnosis of TAH.

An aSID > 42 mmol/L had a PPV of 79.1% in identifying patients with volume-depleted TAH, whereas a value < 39 mmol/L excluded it with a NPV of 76.5%. In patients for whom aSID was inconclusive, a ChU < 15 mmol/L had a PPV of 100% and a NPV of 83.3%, whereas FUA < 12% had a PPV of 85.7% and a NPV of 64.3% in identifying patients with volume-depleted TAH.

In patients with TAH, assessment of aSID, potassium, and chloride in urine can help identifying patients with volume-depleted TAH requiring fluid substitution vs patients with SIAD-like TAH requiring fluid restriction.

Hyponatremia is the most prevalent electrolyte imbalance encountered among hospitalized patients, athletes, the elderly, patients with chronic ailments, postoperative patients, and a few asymptomatic individuals. Clinical manifestations of hyponatremia can be diverse, with characteristic neurological symptoms. Depending on in-depth medical history, physical examination (including volume status assessment), laboratory investigation, and drug history, patients can be classified broadly as undergoing hypervolemic, euvolemic, or hypovolemic hyponatremia. However, patients with hypervolemic hyponatremia often present with distinctive signs such as edema or ascites, and the clinical presentation of hypovolemic and euvolemic hyponatremia poses significant challenges for clinicians. The convolution in clinical manifestations of patients is due to the varied etiologies of euvolemic hyponatremia, such as syndrome of inappropriate antidiuretic hormone secretion (SIADH), adrenocortical insufficiency, hypothyroidism, psychogenic polydipsia, different classes of drugs (chemotherapeutics, antipsychotics, antidepressants), endurance exercise events, and reset osmostat syndrome (ROS). The management of hyponatremia depends on the rate of hyponatremia onset, duration, severity of symptoms, levels of serum sodium, and underlying comorbidities. Over the last decade, the clinical understanding of hyponatremia has been scattered due to the introduction of innovative laboratory markers and new drugs. This article will be a conspectus of all the recent advancements in the field of diagnosis, investigations, management, and associations of hyponatremia, along with traditional clinical practices. Subsequently, a holistic overview has been laid out for the clinicians to better understand and identify knowledge deficiencies on this topic.

Paraneoplastic syndromes are a group of clinical conditions with specific signs and symptoms that are associated with underlying malignancies. The pathophysiology of paraneoplastic syndromes is caused by either the ectopic production of various hormones or the immune production of autoantibodies. Lung cancers are also notorious for being accompanied by paraneoplastic syndromes. The endocrine paraneoplastic syndromes most commonly associated with lung cancer include hypercalcemia of malignancy and syndrome of inappropriate antidiuretic hormone secretion (SIADH). Oftentimes, one of the initial findings in the early stages of lung malignancy is not symptoms of a primary lung neoplasm, but the symptoms and/or lab findings of a paraneoplastic syndrome. This article has been written to present a case of how an asymptomatic patient with a lung mass and lab values suggesting SIADH could benefit from an alteration to the current status quo in the work-up of hypo-osmolar hyponatremia. The main reason for writing the article is to suggest incorporating one of the United States Preventive Services Task Force (USPSTF) guidelines into the current work-up of hypo-osmolar hyponatremia. Currently, the workup for hypo-osmolar hyponatremia says, "consider chest imaging." However, incorporating one of the USPSTF screenings into a questionnaire for medical providers could be beneficial in identifying lung abnormalities sooner in patients with a smoking history and also be more appropriate in determining whether a patient should receive chest imaging.