Treatment Of Hyponatremia In Patients Research Articles

Effects of Short-Term Human Albumin Infusion for the Prevention and Treatment of Hyponatremia in Patients with Liver Cirrhosis.

Background: Human albumin (HA) infusion is potentially effective for the management of hyponatremia in liver cirrhosis, but the current evidence is very limited. Methods: In this retrospective study, 2414 cirrhotic patients who were consecutively admitted to our hospital between January 2010 and June 2014 were included in the Hospitalization outcome cohort, and 339 cirrhotic patients without malignancy who were consecutively admitted to our department between December 2014 and April 2021 were included in the Long-term outcome cohort. The development and improvement of hyponatremia were compared between patients who received HA infusion during hospitalizations and did not. Logistic and Cox regression analyses were performed to evaluate the association of development and improvement of hyponatremia during hospitalizations with the outcomes. Odds ratios (ORs) and hazard ratios (HRs) were calculated. Results: In the two cohorts, HA infusion significantly decreased the incidence of hyponatremia and increased the rate of improvement of hyponatremia in cirrhotic patients during hospitalizations. In the Hospitalization outcome cohort, the development of hyponatremia during hospitalizations was significantly associated with increased in-hospital mortality (OR = 2.493, p < 0.001), and the improvement of hyponatremia during hospitalizations was significantly associated with decreased in-hospital mortality (OR = 0.599, p = 0.014). In the Long-term outcome cohort, the development of hyponatremia during hospitalizations was significantly associated with decreased long-term survival (HR = 0.400, p < 0.001), and the improvement of hyponatremia during hospitalizations was not significantly associated with long-term survival (HR = 1.085, p = 0.813). Conclusions: HA infusion can effectively prevent the development of hyponatremia and improve hyponatremia in cirrhotic patients during hospitalizations, which may influence the patients’ outcomes.

Use of Human Albumin Administration for the Prevention and Treatment of Hyponatremia in Patients with Liver Cirrhosis: A Systematic Review and Meta-Analysis.

Background. Hyponatremia is a common complication of liver cirrhosis and aggravates patients’ outcomes. It may be corrected by human albumin (HA) infusion. Herein, we have conducted a systematic review and meta-analysis to evaluate the efficacy of intravenous HA administration for the prevention and treatment of hyponatremia in liver cirrhosis. Methods. Literature was searched in the PubMed, EMBASE, and Cochrane Library databases. If possible, a meta-analysis would be conducted. Incidence of hyponatremia, rate of resolution of hyponatremia, and serum sodium level were compared between cirrhotic patients who received and did not receive HA infusion. Odds ratios (ORs) or mean differences (MDs) with 95% confidence intervals (CIs) were calculated. The quality of evidence was assessed by the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system. Results. Initially, 3231 papers were identified. Among them, 30 studies, including 25 randomized controlled trials (RCTs) and 5 cohort studies, were eligible. Among cirrhotic patients without hyponatremia, the HA infusion group had significantly lower incidence of hyponatremia (OR = 0.55, 95%CI = 0.38–0.80, p = 0.001) and higher serum sodium level (MD = 0.95, 95%CI = 0.47–1.43, p = 0.0001) as compared to the control group. Among cirrhotic patients with hyponatremia, the HA infusion group had a significantly higher rate of resolution of hyponatremia (OR = 1.50, 95%CI = 1.17–1.92, p = 0.001) as compared to the control group. Generally, the quality of available evidence is low. Conclusions. Based on the current evidence, HA may be considered for preventing the development of hyponatremia in liver cirrhosis, especially in those undergoing LVP, and treating hyponatremia. Well-designed studies are required to clarify the effects of HA infusion on hyponatremia in liver cirrhosis.

Risk of pre-existing hyponatremia and mortality in patients with traumatic brain injury across age groups

Traumatic brain injurySodiumClinical outcomes.

Diagnosis and treatment of hyponatremia in patients with liver cirrhosis

Diagnosis and treatment of hyponatremia in patients with liver cirrhosis

Urea treatment in fluid restriction-refractory hyponatraemia.

Hyponatraemia in hospitalized patients is common and associated with increased mortality. International guidelines give conflicting advice regarding the role of urea in the treatment of SIADH. We hypothesized that urea is a safe, effective treatment for fluid restriction-refractory hyponatraemia. Review of urea for the treatment of hyponatraemia in patients admitted to a tertiary hospital during 2016-2017. Primary end-point: proportion of patients achieving a serum sodium ≥130mmol/L at 72hours. Urea was used on 78 occasions in 69 patients. The median age was 67 (IQR 52-76), 41% were female. Seventy (89.7%) had hyponatraemia due to SIADH-CNS pathology (64.3%) was the most common cause. The duration was acute in 32 (41%), chronic in 35 (44.9%) and unknown in the rest. The median nadir serum sodium was 122mmol/L (IQR 118-126). Fluid restriction was first-line treatment in 65.4%. Urea was used first line in 21.8% and second line in 78.2%. Fifty treatment episodes (64.1%) resulted in serum sodium ≥130mmol/L at 72hours. In 56 patients who received other prior treatment, the mean sodium change at 72hours (6.9±4.8mmol/L) was greater than with the preceding treatments (-1.0±4.7mmol/L; P<0.001). Seventeen patients (22.7%) had side effects (principally distaste), none were severe. No patients developed hypernatraemia, overcorrection (>10mmol/L in 24hours or >18mmol/L in 48hours), or died. Urea is safe and effective in fluid restriction-refractory hyponatraemia. We recommend urea with a starting dose of ≥30g/d, in patients with SIADH and moderate to profound hyponatraemia who are unable to undergo, or have failed fluid restriction.

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

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. 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. 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. 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.

Treatment of Hyponatremia in Patients with Acute Neurological Injury.

Little data exist regarding the practice of sodium management in acute neurologically injured patients. This study describes the practice variations, thresholds for treatment, and effectiveness of treatment in this population. This retrospective, multicenter, observational study identified 400 ICU patients, from 17 centers, admitted for ≥48h with subarachnoid hemorrhage (SAH), traumatic brain injury (TBI), intraparenchymal hemorrhage, or intracranial tumors between January 1, 2011 and July 31, 2012. Data collection included demographics, APACHE II, Glascow Coma Score (GCS), serum sodium (Na+), fluid rate and tonicity, use of sodium-altering therapies, intensive care unit (ICU) and hospital length of stay, and modified Rankin score upon discharge. Data were collected for the first 21days of ICU admission or ICU discharge, whichever came first. Sodium trigger for treatment defined as the Na+ value prior to treatment with response defined as an increase of ≥4mEq/L at 24h. Sodium-altering therapy was initiated in 34% (137/400) of patients with 23% (32/137) having Na+ >135mEq/L at time of treatment initiation. The most common indications for treatment were declining serum Na+ (68/116, 59%) and cerebral edema with mental status changes (21/116, 18%). Median Na+ treatment trigger was 133mEq/L (IQR 129-139) with no difference between diagnoses. Incidence and treatment of hyponatremia was more common in SAH and TBI [SAH (49/106, 46%), TBI (39/97, 40%), ICH (27/102, 26%), tumor (22/95, 23%); p=0.001]. The most common initial treatment was hypertonic saline (85/137, 62%), followed by oral sodium chloride tablets (42/137, 31%) and fluid restriction (15/137, 11%). Among treated patients, 60% had a response at 24h. Treated patients had lower admission GCS (12 vs. 14, p=0.02) and higher APACHE II scores (12 vs. 10, p=0.001). There was no statistically significant difference in outcome when comparing treated and untreated patients. Sodium-altering therapy is commonly employed among neurologically injured patients. Hypertonic saline infusions were used first line in more than half of treated patients with the majority having a positive response at 24h. Further studies are needed to evaluate the impact of various treatments on patient outcomes.

Mutation in the V2 vasopressin receptor gene, AVPR2, causes nephrogenic syndrome of inappropriate diuresis

Nephrogenic syndrome of inappropriate antidiuresis (NSIAD) is a recently discovered rare disease caused by gain-of-function mutations of the V2 vasopressin receptor gene, AVPR2. To date, mutations of Phe229 and Arg137 have been identified as gain-of-function in the V2 vasopressin receptor (V2R). These receptor mutations lead to hyponatremia, which may lead to clinical symptoms in infants. Here we present a newly identified I130N substitution in exon 2 of the V2R gene in a family, causing NSIAD. This I130N mutation resulted in constitutive activity of the V2R with constitutive cyclic adenosine monophosphate (cAMP) generation in HEK293 cells. This basal activity could be blocked by the inverse agonist tolvaptan and arginine-vasopressin stimulation enhanced the cAMP production of I130N-V2R. The mutation causes a biased receptor conformation as the basal cAMP generation activity of I130N does not lead to interaction with β-arrestin. The constitutive activity of the mutant receptor caused constitutive dynamin-dependent and β-arrestin-independent internalization. The inhibition of basal internalization using dominant-negative dynamin resulted in an increased cell surface expression. In contrast to the constitutive internalization, agonist-induced endocytosis was β-arrestin dependent. Thus, tolvaptan could be used for treatment of hyponatremia in patients with NSIAD who carry the I130N-V2R mutation.

GW24-e3948 Evaluation of Tolvaptan in the treatment of hyponatremia in chronic heart failure patient

ObjectivesTo evaluate the efficacy and safety of tolvaptan in the treatment of hyponatremia in patients with chronic heart failure.MethodsScreening enrolled 16 patients with chronic heart failure (≥18y), and they were...

Hyponatremia and cancer: Results of a retrospective analysis of 45 patients treated with a short course of low-dose tolvapan.

e20705 Background: Hyponatremia in the cancer patient is usually caused by the syndrome of inappropriate antidiuretic hormone (SIADH). Other factors may cause hypovolemic hyponatremia, diarrhea, and vomiting. It’s present in 47% of cancer admissions. Introduction of vaptans acting as V2-receptor antagonists considerably improved the unconvincing results of conventional treatment consisting of fluid restriction potentially combined with sodium supplementation and/or demeclocycline therapy. Methods: We present a retrospective analysis of hyponatremic cancer patients treated with Tolvaptan. 45 patients, [31 men 14 women], median age 69 years old. 31.1 % had lung cancer, 17,6% other tumors, 11,1% colorectal and 11,1% prostate cancer. Histology: 53,3% Adenocarinoma, 15,6% SCLC, 15,2% others and 5,6% Epidermoid.The mean of the lowest sodium level was associated with squamous histology (Na 118 mEq/L). Descriptively, older patients (&gt;66 y) had lower levels of Na compared to those younger than 66y (Na 122 mEq/L vs Na124 mEq/L). Median of Na at diagnosis of hyponatremia was 124 mEq/L,"waiting period" days before starting treatment,1d (SD= 1,745). Duration treatment [ Sodium levels out of risk according to the doctor criteria]. Results: Participants improved significantly after treatment period (p=.000). There were no differences in TOLVAPTAN improvements between patients with ≤ 124 mEq/L vs &gt;124 mEq/L (p=.142), but patients with Na ≤ 124 mEq/L tend to achieved higher levels of sodium at the end of treatment (p=.016). No significant differences between different histology, location, "waiting period", duration of treatment, or age. However, Men significantly improved after treatment with tolvaptan (p=.000) and women do not showed significant changes (p=.753) (women had significantly higher pretreatment sodium level than men (122.4 mEq/L vs. 126.2 mEq/L,(p= .05). Conclusions: Tolvaptan is effective in the treatment of hyponatremia in patients with differents histological cancers especially with levels lower than 124 mEq/L. Tolvaptan had good safety profile with no side effects. A short course of two days and low dose (15mg/p.o./d ) with Tolvaptan restored safe Sodium levels.

Syndrome of inappropriate antidiuresis and cerebral salt wasting syndrome: are they different and does it matter?

The syndrome of inappropriate antidiudresis (SIAD) and cerebral salt wasting (CSW) are similar conditions with the main difference being the absence or presence of volume depletion. The two conditions may be indistinguishable at presentation, as volume status is difficult to assess, which can lead to under-diagnosis of CSW in patients with central nervous system (CNS) disease. Carefully conducted studies in patients with CNS disease have indicated that CSW may be more common than SIAD. CSW may be differentiated from SIAD based on the persistence of hypouricemia and increased fractional excretion of urate following the correction of hyponatremia. Hyponatremia should be prevented if possible and treated promptly when discovered in patients with CNS disease as even mild hyponatremia could lead to neurological deterioration. Fluid restriction should not be used for the prevention or treatment of hyponatremia in hospitalized patients with CNS disease as it could lead to volume depletion especially if CSW is present. 0.9% sodium chloride may not be sufficiently hypertonic for the prevention of hyponatremia in hospitalized patients with CNS disease and a more hypertonic fluid may be required. The preferred therapy for the treatment of hyponatremia in patients with CNS disease is 3% sodium chloride.

Vasopressin-2 Antagonists for Treatment of Hyponatremia in Cirrhosis - A Systematic Review and Meta-Analysis

Purpose: Hyponatremia is a common electrolyte abnormality in patients with cirrhosis and affects their outcome. Vasopressin-2 (V2) receptor antagonists increase free water clearance and are useful for treatment of hyponatremia. Randomized controlled trials (RCTs) have shown conflicting data on efficacy and safety of V2 receptor antagonists in the treatment of hyponatremia in cirrhotic patients. A systematic review and meta-analysis of all RCTs was performed to assess safety and efficacy of V2 receptor antagonists in the treatment of hyponatremia in patients with cirrhosis. Methods: Pub Med, Ovid, Cochrane reviews, EMBASE and ISI web of science databases were searched for all RCTs on treatment of hyponatremia using V2 receptor antagonists. Studies including patients with hyponatremia of different causes but not reporting data on cirrhotics were excluded. Data was extracted into a predefined Excel spreadsheet for patient demographics, sample size (in treated and control patients), type and dose of V2 receptor antagonist, change [post treatment - baseline (mean±SD)] on various outcomes (Table), and adverse effects. Data were entered into comprehensive meta-analysis 9.2 software and analyzed using random effects model. Heterogeneity and publication bias across the studies (reported if > 2 studies) were assessed using Chi-2 and Egger's tests respectively. Meta-regression was performed to assess heterogeneity for year of publication, type and dose of drug, baseline serum sodium, time at which change is reported (12-168 hrs), and percent males.Table: [324] Pooled data on vasopressin-2 receptor antagonists for treatment of hyponatremia in cirrhosisResults: Total 6 studies (n=342, 169 treated) were analyzed. Pooled data showed a significant increase in serum sodium with a decrease in urine osmolality (Table). However, there was no change in other parameters. The drugs were safe with similar proportion of patients among treated and control groups experiencing adverse effects with pooled OR of 1.29 (95% CI 0.73-2.25); P=0.93. Most common side effect was increased thirst. There was marked heterogeneity but no publication bias across the studies. Meta regression showed that the year of study publication along with type and dose of the drug contributed to data heterogeneity. Conclusion: Vasopressin-2 receptor antagonists are effective and safe for treatment of hyponatremia in patients with cirrhosis. Further studies are needed to determine efficacy and safety of long-term use of vasopressin receptor antagonists for treatment of hyponatremia in patients with cirrhosis.

Tolvaptan: a new tool for the effective treatment of hyponatremia in psychotic disorders

Importance of the field: Hyponatremia (serum sodium concentration < 136 mEq/liter) is a common and potentially life-threatening medical comorbidity seen in patients with psychotic disorders. Tolvaptan, a selective antagonist of the V2-receptor, is FDA-approved for the treatment of clinically significant hypervolemic and euvolemic hyponatremia. This represents a major development in the care of psychotic individuals with hyponatremia.Areas covered in the review: This review provides an overview of the existing literature on prevalence rates and risk factors associated with hyponatremia in psychotic patients (1923 – present). Tolvaptan is discussed as a potential advance in the treatment of hyponatremia in patients with psychotic disorders, and preliminary data are reviewed.What the reader will gain: The reader will gain an appreciation of the prevalence of hyponatremia among psychotic individuals, an understanding of the distinctions between acute and chronic hyponatremia in this population, and awareness that effective treatments are becoming available.Take home message: A modest literature exists regarding prevalence rates and risk factors associated with hyponatremia in psychotic populations. Hyponatremia is common and serious enough to merit clinical concern. Perhaps, now that tolvaptan has been FDA-approved, progress will accelerate and new insights will develop that begin to bring relief from this medical comorbidity among psychotic patients.

Conivaptan, a Vasopressin-Receptor Antagonist, for the Treatment of Hyponatremia in Patients with and without Underlying Heart Failure

Conivaptan, a Vasopressin-Receptor Antagonist, for the Treatment of Hyponatremia in Patients with and without Underlying Heart Failure