Efectividad de la administración de urea para el tratamiento de la hiponatremia en la insuficiencia cardiaca / Effectiveness of urea administration for the treatment of hyponatremia in heart failure

Objetivos Valorar la eficacia y la seguridad de la urea en pacientes con hiponatremia e insuficiencia cardiaca (IC). Métodos y resultados Se trata de un estudio observacional retrospectivo analítico de pacientes con IC e hiponatremia (Na+ <135mmol/l). Se incluyeron 49 pacientes tratados con urea y 47 pacientes que no recibieron urea, todos ellos bajo tratamiento estándar (según práctica clínica habitual) de la IC, con seguimiento en el hospital Álvaro Cunqueiro de Vigo entre enero de 2013 y mayo de 2022. En el estudio se evaluó la normalización de los niveles de sodio (Na >135mmol/l). La natremia al inicio del tratamiento con urea oral era de 127±5,22mmol/l, a las 24horas el sodio era de 128±2,47 (p<0,009) y la media el día de la normalización fue de 135,19±4,23mmol/l (p<0,005). Los días de media para conseguir la normalización del sodio fueron 5,03±2,37. La uremia al inicio del tratamiento con urea era de 73±46,93mg/dl y la media el día de la normalización del Na+ fue de 116,05±63,64mg/dl (p<0,002). La dosis media de urea oral fue 22,5g/día. No se observaron efectos adversos relevantes, ni cambios en cuanto a las cifras de creatinina. Conclusiones El tratamiento con urea oral añadido al tratamiento estándar, durante cortos periodos de tiempo, es seguro y eficaz para corregir la natremia en pacientes con IC hipervolémica con hiponatremia.

Objectives To assess the efficacy and safety of urea in patients with hyponatremia and heart failure (HF). Methods and results This is a retrospective observational analytical study of patients with HF and hyponatremia (Na+ <135mmol/L). Forty-nine patients treated with urea and 47 patients who did not receive urea, all under standard treatment (according to usual clinical practice) for HF, were included and followed up at Álvaro Cunqueiro Hospital in Vigo (Spain) between January 2013 and May 2022. The study evaluated the normalization of sodium levels (Na >135mmol/L). The initial natremia at the start of oral urea treatment was 127±5.22 mmol/L, at 24h the sodium level was 128±2.47 (P<.009), and the mean on the day of normalization was 135.19±4.23mmol/L (P<.005). The average number of days to achieve sodium normalization was 5.03±2.37 days. The initial uremia at the start of urea treatment was 73±46.93mg/dL, and the mean on the day of Na+ normalization was 116.05±63.64mg/dL (P<.002). The average oral urea dose was 22.5g/day. No relevant adverse effects were observed, nor were there significant changes in creatinine levels. Conclusions Oral urea treatment, when added to standard treatment for short periods of time, is safe and effective in correcting natremia in patients with hypervolemic HF with hyponatremia. (AU)

Palatability of two different formulations of urea for the treatment of hyponatremia: A double-blind, randomized, cross-over study.

BACKGROUND AND AIMS: Hyponatremia (HN) is the most common disorder of electrolytes encountered in clinical practice. Considering that HN is associated with high morbidity and mortality, it is important to identify treatments for these patients. The therapeutic approaches for HN depend on the severity and the character of the pathology (acute vs. chronic). Among intervention strategies, oral urea represents an effective, safe, and well-tolerated therapeutic approach in the management of chronic hyponatremia. Oral ureal is commonly prepared as a galenic formulation that is usually associated with distaste problems. A double-blind, randomized, cross-over clinical trial was conducted to evaluate and compare the palatability of two different urea formulations: a commercial urea formulation and a galenic one (trial registered on www.isrctn.com, number: ISRCTN18369035). MATERIALS AND METHODS: Thirty-six healthy subjects (18 female and 18 male, median age 55 years) were enrolled in the study and randomized to consume 7 g of formulation A (commercial formulation) or formulation B (galenic formulation) twice a day away from meals, solubilizing the products in 125 mL of water (T0). After three days of a wash-out, the formulations were crossed-over and consumed twice a day away from meals (T4). After the consumption of products, both in the morning and the evening, participants completed a specific questionnaire to evaluate the products' palatability. RESULTS: The commercial formulation was globally more appreciated than the galenic one, in terms of smell, taste, and aftertaste. The commercial formulation was better accepted as a potential treatment in 44 % of subjects compared to 14 % of subjects for galenic formulation. CONCLUSIONS: The clinical trial confirmed the better palatability of the commercial oral urea formulation, containing citrus flavor, which therefore represents a therapeutic strategy that could improve adherence to the therapy in chronic patients with hyponatremia.

SSRI/SNRI -induced Hyponatremia: A Case Series of 26 Patients in a Single Institution from 2018 to 2020.

Antidepressant medications are widely used by patients with depression or a depressive disorder. In spite of a generally favorable safety profile of selective serotonin reuptake inhibitors or serotonin - norepinephrine reuptake inhibitors (SSRI/SNRI), several cases of a possible connection between SSRI/SNRI and hyponatremia have been reported. To describe the clinical characteristics of patients with hyponatremia after SSRI/SNRI exposure, and to examine the association between SSRI/SNRI exposure and the presence of hyponatremia in a Chinese population. A retrospective single-center case series study. We performed a retrospective evaluation of inpatients with SSRI/SNRI-induced hyponatremia from a single institution in China between 2018 and 2020. Clinical data were obtained through review of medical records. Patients who met the initial inclusion criteria but did not develop hyponatremia acted as controls. The study was approved by the Clinical Research Ethics Board of Beijing Hospital (Beijing, P.R. China). We identified 26 patients with SSRI/SNRI-induced hyponatremia. The incidence rate of hyponatremia was 1.34% (26/1937) in the study population. The mean age at diagnosis was 72.58 (±12.84) years, with a male: female ratio of 1:1.42. The duration between SSRI/SNRI exposure and the onset of hyponatremia was 7.65 (±4.88) days. The minimum serum sodium level was 2328.23 (±107.25) mg/dL in the study group. Seventeen patients (65.38%) received sodium supplements. Four patients (15.38%) switched to another antidepressant. Fifteen patients (57.69%) recovered by the time of discharge. There were significant differences in serum potassium, serum magnesium and serum creatinine level between the two groups (p < 0.05). The rate of use of sertraline was significantly higher in the study group compared with the control group (p < 0.05). This pattern was not found in other SSRI/SNRI (p > 0.05). The results of our study show that SSRI/SNRI exposure, in addition to hyponatremia, may also affect the level of serum potassium, serum magnesium and serum creatinine. A history of hyponatremia and exposure to SSRI/SNRI may be potential risk factors for the development of hyponatremia. Future prospective studies are needed to validate these findings.

Oral Urea Supplementation in the Treatment of Acute Hyponatremia among Hospitalized Adults: A Systematic Review.

Hyponatremia is the most common electrolyte disturbance among hospitalized adults. Oral urea is currently recommended in Europe in the treatment of chronic hyponatremia; no published systematic review investigating oral urea for acute hyponatremia among hospitalized adults exists. An oral urea supplement became available in the United States in 2016. This was a systematic review investigating the use of oral urea in the treatment of acute hyponatremia among hospitalized adults. Pubmed, CINAHL, Scopus, Web of Science, and Cochrane databases were searched for studies published between 1998 and 2021. Risk of bias was assessed using the ROBINS-I tool; strength of the evidence was assessed using GRADE criteria. Changes in serum sodium and measures of safety and tolerance were reported. Eight studies were identified that met inclusion criteria, which included a total of 296 patients. Seven studies were retrospective. All studies found an increase in serum sodium levels associated with oral urea supplementation. Side effects were minimal; one patient discontinued urea due to a side effect (dysgeusia). Urea dose/duration varied among the studies. Based on the serious risk of bias and GRADE criteria, the strength of the evidence was considered low. Oral urea supplementation was associated with increases in serum sodium concentrations among hospitalized adults with hyponatremia, and appears to be safe and well tolerated in this population. Prospective controlled trials are needed to establish the efficacy, comparative effectiveness, and potential cost savings of this therapy.Key teaching pointsHyponatremia is associated with negative clinical outcomes among hospitalized adults.Oral urea is now available in the United States, and is currently recommended in Europe to treat chronic hyponatremia.This systematic review shows that oral urea supplementation may be associated with increases in serum sodium levels among hospitalized adults with hyponatremia, and appears safe and well-tolerated; however, the studies reviewed here are at high risk of bias and the available evidence is of low quality, making any recommendation drawn from this data weak.Prospective controlled trials are needed to establish the efficacy, comparative effectiveness, and potential cost savings of oral urea supplementation for hyponatremia.

Hyponatremia Associated With Standard-Dose Trimethoprim-Sulfamethoxazole Use in an Immunocompetent Patient.

INTRODUCTION: Trimethoprim-sulfamethoxazole (TMP-SMX) use in immunocompromised patients can cause dose-dependent electrolyte irregularities including hyponatremia, hyperkalemia, and metabolic acidosis. We report a case of isolated hyponatremia caused by low-dose TMP-SMX use in an immunocompetent patient that mimicked the syndrome of inappropriate antidiuretic hormone secretion (SIADH). CASE PRESENTATION: A 72-year-old woman was admitted to the hospital for acute onset of weakness and ambulatory dysfunction after starting TMP-SMX (160 mg/800 mg). She was found hyponatremic (sodium level, 125 mmol/L, down from 141 mmol/L prior to medication initiation). After ruling out diuretics use, and adrenal and thyroid dysfunction, we started her on intravenous saline infusion to manage her TMP-SMX-induced hyponatremia, and her symptoms resolved. DISCUSSION: Electrolyte problems in immunocompromised patients treated for opportunistic infections with high-dose TMP-SMX (≥ 8 mg/kg/d TMP) are well-documented. However, the effects in immunocompetent patients are uncommon when standard dose (< 8 mg/kg/d TMP) is used. CONCLUSIONS: TMP-SMX blocks the aldosterone-mediated sodium reabsorption in the collecting ducts, and the trimethoprim component itself is structurally similar to potassium-sparing diuretics, which block sodium uptake at the distal nephron-both of which can cause hyponatremia.

A snake toxin as a theranostic agent for the type 2 vasopressin receptor.

Rationale: MQ1, a snake toxin which targets with high nanomolar affinity and absolute selectivity for the type 2 vasopressin receptor (V2R), is a drug candidate for renal diseases and a molecular probe for imaging cells or organs expressing V2R. Methods: MQ1's pharmacological properties were characterized and applied to a rat model of hyponatremia. Its PK/PD parameters were determined as well as its therapeutic index. Fluorescently and radioactively labeled MQ1 were chemically synthesized and associated with moderate loss of affinity. MQ1's dynamic biodistribution was monitored by positron emission tomography. Confocal imaging was used to observe the labeling of three cancer cell lines. Results: The inverse agonist property of MQ1 very efficiently prevented dDAVP-induced hyponatremia in rats with low nanomolar/kg doses and with a very large therapeutic index. PK (plasma MQ1 concentrations) and PD (diuresis) exhibited a parallel biphasic decrease. The dynamic biodistribution showed that MQ1 targets the kidneys and then exhibits a blood and kidney biphasic decrease. Whatever the approach used, we found a T1/2α between 0.9 and 3.8 h and a T1/2ß between 25 and 46 h and demonstrated that the kidneys were able to retain MQ1. Finally, the presence of functional V2R expressed at the membrane of cancer cells was, for the first time, demonstrated with a specific fluorescent ligand. Conclusion: As the most selective V2 binder, MQ1 is a new promising drug for aquaresis-related diseases and a molecular probe to visualize in vitro and in vivo V2R expressed physiologically or under pathological conditions.

Glucocorticoids Reverse Diluted Hyponatremia Through Inhibiting Arginine Vasopressin Pathway in Heart Failure Rats.

Background Arginine vasopressin dependent antidiuresis plays a key role in water-sodium retention in heart failure. In recent years, the role of glucocorticoids in the control of body fluid homeostasis has been extensively investigated. Glucocorticoid deficiency can activate V2R (vasopressin receptor 2), increase aquaporins expression, and result in hyponatremia, all of which can be reversed by glucocorticoid supplement. Methods and Results Heart failure was induced by coronary artery ligation for 8 weeks. A total of 32 rats were randomly assigned to 4 groups (n=8/group): sham surgery group, congestive heart failure group, dexamethasone group, and dexamethasone in combination with glucocorticoid receptor antagonist RU486 group. An acute water loading test was administered 6 hours after drug administration. Left ventricular function was measured by a pressure-volume catheter. Protein expressions were determined by immunohistochemistry and immunoblotting. The pressure-volume loop analysis showed that dexamethasone improves cardiac function in rats with heart failure. Western blotting confirmed that dexamethasone remarkably reduces the expressions of V2R, aquaporin 2, and aquaporin 3 in the renal-collecting ducts. As a result of V2R downregulation, the expressions of glucocorticoid regulated kinase 1, apical epithelial sodium channels, and the furosemide-sensitive Na-K-2Cl cotransporter were also downregulated. These favorable effects induced by dexamethasone were mostly abolished by the glucocorticoid receptor inhibitor RU486, indicating that the aforementioned effects are glucocorticoid receptor mediated. Conclusions Glucocorticoids can reverse diluted hyponatremia via inhibiting the vasopressin receptor pathway in rats with heart failure.

[A case of tuberculous meningitis with pleural effusion as a manifestation of a paradoxical reaction during anti-tuberculosis therapy].

We present a case of tuberculous meningitis (TBM), wherein pleural effusion developed as a manifestation of paradoxical reaction during anti-tuberculosis therapy. An 87-year-old diabetic man was referred to our clinic for fever and impaired consciousness. He did not obey vocal commands. No ocular motor deficit, facial palsy, or limb weakness was observed. He had hyponatremia due to inappropriate antidiuresis. Examination of the cerebrospinal fluid revealed lymphocytosis and high adenosine deaminase (ADA) activity, suggestive of TBM. He was treated with isoniazid, rifampicin, and pyrazinamide, after which his symptoms quickly resolved. Lymphocyte count, ADA activity, and protein concentration in the cerebrospinal fluid decreased. However, approximately 30 days after the initiation of therapy, he developed mild hypoxemia. A chest CT scan revealed pleural effusion. The pleural fluid was exudate with elevated ADA activity, which was consistent with tuberculous pleural effusion. Shortly after the use of a herbal medicine, Goreisan extract, hyponatremia and hypoproteinemia improved, and the pleural effusion was reduced. Approximately one-third of patients with TBM are reported to develop a paradoxical reaction, such as tuberculoma, hydrocephalus, and optochiasmatic and spinal arachnoiditis. The present case suggests that extra-central nervous system manifestations, including pleural effusion, should be considered when treating TBM.

Clinical characteristics of autoimmune GFAP astrocytopathy.

The clinical features of autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy remain to be elucidated. We describe here the clinical features of 14 patients with GFAP astrocytopathy confirmed by detection of GFAP-IgG in cerebrospinal fluid (CSF). The novel findings of this study are as follows. First, over half of the patients presented with movement disorders (tremor, myoclonus, and ataxia), autonomic dysfunction (mainly urinary dysfunction), and hyponatremia. Second, most patients showed transient elevation of adenosine deaminase activity levels in CSF. Finally, some patients showed bilateral hyperintensities in the posterior part of the thalamus on brain magnetic resonance imaging.

Prevention and Treatment of Hyponatremia in Patients with Subarachnoid Hemorrhage: A Systematic Review.

BACKGROUND: Current guidelines for the management of hyponatremia in patients with subarachnoid hemorrhage (SAH) are not based on a systematic assessment of the literature. We evaluated published studies on the efficacy and safety of current preventative and treatment strategies for hyponatremia in patients with SAH. METHODS: We searched the Cochrane Central Register of Controlled Trials, Embase, MEDLINE, and PubMed for relevant studies. Primary outcomes of interest included neurologic functional outcomes, symptomatic vasospasm, and others. Secondary outcomes included measures of sodium and volume status. RESULTS: We included 5 out of 117 identified studies: 1 before-and-after observational trial (using fludrocortisone) and 4 randomized controlled trials (2 using fludrocortisone; 2 using hydrocortisone). All 5 trials had a high risk of bias in at least 1 domain. We could not perform a meta-analysis of functional outcomes; however, individual studies did not demonstrate statistically significant differences. Mineralocorticoid use did not statistically significantly reduce the incidence of symptomatic vasospasm (relative risk, 0.60; 95% confidence interval, 0.35-1.03; I2 = 0%). The studies did not report other primary outcomes. In the 4 RCTs, mineralocorticoid use reduced natriuresis and volume contraction. CONCLUSIONS: Current evidence does not demonstrate a benefit of preventative treatment with mineralocorticoids in clinically important outcomes, although a difference cannot be ruled out due to imprecision. Larger well-designed trials are needed to establish the impact of mineralocorticoids and fluid and sodium supplementation strategies on clinically relevant outcomes in the prevention and treatment of hyponatremia in patients with SAH.

Effect of single-dose of tolvaptan in neurocritical patients with hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion / Efecto de una dosis única de tolvaptán en pacientes neurocríticos con hiponatremia debido a SIADH

No disponible

Hyponatremia in an Elderly Patient due to Isolated Hypoaldosteronism Occurring after Licorice Withdrawal.

Hyponatremia is one of the most common electrolyte disorders encountered in the elderly. We present the case of an 81-year-old man who developed hyponatremia due to isolated hypoaldosteronism occurring after licorice withdrawal. He had severe hypokalemia with hypertension and was diagnosed with pseudoaldosteronism. He had been taking a very small dose of licorice as a mouth refresher since his early adulthood. Five months after licorice withdrawal, he developed hypovolemic hyponatremia, which was resolved with administration of fludrocortisone acetate. Our experience with this case suggests that isolated hypoaldosteronism occurring after licorice withdrawal should be considered as a potential cause of hyponatremia in elderly patients.

Corticosteroids in the Management of Hyponatremia, Hypovolemia, and Vasospasm in Subarachnoid Hemorrhage: A Meta-Analysis.

BACKGROUND: Cerebral vasospasm and sodium and fluid imbalances are common sequelae of aneurysmal subarachnoid hemorrhage (SAH) and cause of significant morbidity and mortality. Studies have shown the benefit of corticosteroids in the management of these sequelae. We have reviewed the literature and analyzed the available data for corticosteroid use after SAH. METHODS: PubMed, EMBASE, and Cochrane electronic databases were searched without language restrictions, and 7 observational, controlled clinical studies of the effect of corticosteroids in the management of SAH patients were identified. Data on sodium and fluid balances, symptomatic vasospasm (SVS), and outcomes were pooled for meta-analyses using the Mantel-Haenszel random effects model. RESULTS: Corticosteroids, specifically hydrocortisone and fludrocortisone, decreased natriuretic diuresis and incidence of hypovolemia. Corticosteroid administration is associated with lower incidence of SVS in the absence of nimodipine, but does not alter the neurological outcome. CONCLUSIONS: Supplementation of corticosteroids with mineralocorticoid activity, such as hydrocortisone or fludrocortisone, helps in maintaining sodium and volume homeostasis in SAH patients. Larger trials are warranted to confirm the effects of corticosteroids on SVS and patient outcomes.

Extrapontine myelinolysis manifested selectively by acute severe parkinsonian syndrome. Case Report.

OBJECTIVES: Osmotic demyelination syndrome (ODMS) is a rare and serious neurologic disorder with acute myelin disintegration, usually in the pontine area (central pontine myelinolysis) and to a lesser extent, even in other areas of the central nervous system (extrapontine myelinolysis). The main underlying mechanism is the change of serum osmolality with quick correction of low mineral levels, mainly hyponatraemia. Clinical manifestation is various and depends on the localization. DESIGN: We describe an acute isolated extrapontine myelinolysis causing acute onset of parkinsonism in a 61-year-old man who developed quickly progressing parkinsonian syndrome after the rapid correction of hyponatraemia. RESULTS: Brain MRI revealed lesions only in the striatum, sparing the globus pallidus. Substitution therapy with high doses of levodopa significantly improved his clinical condition. CONCLUSION: Extrapontine myelinolysis with isolated affection of basal ganglia is extremely rare. In such case, clinical manifestation of acute severe parkinsonism could be successfully treated by high dose of levodopa.

Successful treatment of a cat with primary hypoadrenocorticism and severe hyponatremia with desoxycorticosterone pivalate (DOCP).

A 6-year-old, castrated male Siamese cat was diagnosed with primary hypoadrenocorticism, confirmed by an adrenocorticotopic hormone (ACTH) stimulation test documenting both hypocortisolism and hypoaldosteronism. The cat was successfully treated using a combination of prednisolone and desoxycorticosterone pivalate (DOCP). This case demonstrates that DOCP can be used successfully as mineralocorticoid supplementation in cats with hypoadrenocorticism and may have a longer therapeutic duration than that in dogs.

Traitement réussi d'un chat atteint d'hypoadrénocorticisme primaire et d'hyponatrémie à l'aide de pivalate de désoxycorticostérone (DOCP). Un diagnostic d'hypoadrénocorticisme primaire a été posé pour un chat Siamois castré âgé de 6 ans et confirmé par un test de stimulation de l'hormone adrénocorticotope (ACTH) qui a documenté l'hypocortisolisme et l'hypoaldostéronisme. Le chat a été traité avec succès à l'aide d'une combinaison de prednisolone et de pivalate de désoxycorticostérone (DOCP). Ce cas démontre que le DOCP peut être utilisé avec succès en tant que supplément de minéralocorticoïdes chez les chats atteints d'hypoadrénocorticisme et peut présenter une durée thérapeutique plus longue que chez les chiens.(Traduit par Isabelle Vallières).

La urea en el manejo del síndrome de secreción inadecuada de la ADH: una revisión sistemática de la literatura / Urea for management of the syndrome of inappropriate secretion of ADH: A systematic review

Recientemente se ha propuesto el uso de la urea como tratamiento complementario en el síndrome de secreción inadecuada de la ADH (SIADH). El objetivo del estudio es realizar una revisión de los niveles de evidencia de la urea en el tratamiento de la hiponatremia asociado al SIADH. Se realizó una revisión sistemática de la evidencia a partir de estudios experimentales de acuerdo con la escala propuesta por SIGN. No se encontraron ensayos clínicos. Los 6 estudios analizados presentan carencias metodológicas importantes y están muy sujetos a sesgos. En conclusión, no existe evidencia que sustente el uso de la urea en la hiponatremia asociada al SIADH. Urea has been recently proposed for the management of hyponatremia linked to the syndrome of inappropriate secretion of ADH (SIADH). The objective of the study was to review the levels of evidence for treatment of hyponatremia associated with SIADH with urea. We performed a: systematic review of experimental trials and grading according to SIGN. No clinical trials were found. The 6 studies analysed had methodological limitations and were prone to biases. In conclusion, there is no evidence to support the efficacy of urea for the treatment of hyponatremia following SIADH

Urea has been recently proposed for the management of hyponatremia linked to the syndrome of inappropriate secretion of ADH (SIADH). The objective of the study was to review the levels of evidence for treatment of hyponatremia associated with SIADH with urea. We performed a: systematic review of experimental trials and grading according to SIGN. No clinical trials were found. The 6 studies analysed had methodological limitations and were prone to biases. In conclusion, there is no evidence to support the efficacy of urea for the treatment of hyponatremia following SIADH. Urea has been recently proposed for the management of hyponatremia linked to the syndrome of inappropriate secretion of ADH (SIADH). The objective of the study was to review the levels of evidence for treatment of hyponatremia associated with SIADH with urea. We performed a: systematic review of experimental trials and grading according to SIGN. No clinical trials were found. The 6 studies analysed had methodological limitations and were prone to biases. In conclusion, there is no evidence to support the efficacy of urea for the treatment of hyponatremia following SIADH

Total body sodium depletion and poor weight gain in children and young adults with an ileostomy: a case series.

Patients with high-output small bowel ostomies are at risk for total body sodium depletion (TBSD), defined as a urine sodium level <10 mmol/L. Failure to thrive (FTT) as a consequence of TBSD has been reported in neonates with ileostomies; however, this has not been well described in older children. The records of all children beyond the age of infancy with a small bowel ostomy cared for in our Children's Intestinal Rehabilitation Program from 2010-2012 were reviewed. Four patients between the ages of 18 months and 19 years were identified as having TBSD. All 4 patients experienced unintentional weight loss, despite adequate energy intake based on calculated needs, which was associated with a urine sodium level ≤10 mmol/L. With the supplementation of sodium, either enteral or intravenous, all patients demonstrated improved weight gain and correction of TBSD. The following cases suggest that the relationship between TBSD and FTT may extend well beyond the neonatal period and possibly into adulthood. We advise that patients of all ages with high stoma output have routine urine sodium levels checked, particularly in the setting of weight loss or poor gain. Furthermore, instances of TBSD should be treated with sodium supplementation. Further research is needed to better understand the relationship between TBSD and FTT and to establish intervention guidelines.

Impending cardiac tamponade caused by salt supplement in a hyponatremic patient with chronic kidney disease.

We documented a hyponatremic patient who developed imminent cardiac tamponade upon oral salt supplement. A 72-year-old diabetic woman had hemorrhagic stroke; pericardial effusion; and chronic kidney disease, stage IV. She developed hyponatremia (serum sodium level, 125 mmol/L), compatible with the syndrome of inappropriate antidiuretic hormone, and received oral salt supplement 9 g/d for 4 days. Shortness of breathing and increasing heart rate ensued, and the echocardiography found accumulation of pericardial effusion with signs of impending cardiac tamponade. Pig-tail drainage through pericardiocentesis was done, and the vital signs were stabilized. We found the production of pericardial effusion increased from 100 to 220 mL/d after oral salt supplement at 3 g/d was reassumed. We discuss the relationship between serum sodium levels, the dose of salt supplement and the accumulation of pericardial effusion.