Chronic liver disease (CLD) is a major global health problem and remains an important cause of morbidity, mortality, and healthcare utilization worldwide. It encompasses a broad spectrum of progressive liver disorders characterized by persistent hepatic inflammation, fibrosis, and architectural distortion, eventually leading to cirrhosis and liver failure. The most common etiologies include alcohol-associated liver disease, chronic viral hepatitis, non-alcoholic fatty liver disease, autoimmune liver diseases, and metabolic disorders(1,2). As liver disease progresses, patients transition from a compensated stage, in which hepatic function is relatively preserved, to a decompensated stage marked by the development of complications such as ascites, hepatic encephalopathy, variceal hemorrhage, spontaneous bacterial peritonitis, and hepatorenal syndrome. This transition significantly worsens prognosis and substantially increases the risk of hospitalization and death (3,4). Hyponatremia is one of the most frequent electrolyte abnormalities encountered in patients with advanced chronic liver disease, particularly among those with cirrhosis and portal hypertension. It is primarily dilutional in nature and results from impaired renal free water excretion rather than total body sodium depletion (5,6). Progressive portal hypertension causes marked splanchnic vasodilatation and a reduction in effective arterial blood volume, leading to activation of the renin–angiotensin–aldosterone system, sympathetic nervous system, and non-osmotic release of arginine vasopressin. These neurohormonal adaptations promote renal water retention, resulting in dilutional hyponatremia. The severity of hyponatremia generally parallels the severity of hepatic dysfunction and circulatory impairment (7,8). Serum sodium concentration has emerged as an important prognostic marker in chronic liver disease. Numerous studies have demonstrated that low serum sodium levels are associated with increased incidence of ascites, refractory ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatorenal syndrome, prolonged hospital stay, and increased short-term mortality (9). Hyponatremia also adversely affects quality of life by contributing to fatigue, cognitive dysfunction, muscle cramps, gait disturbances, and an increased risk of falls (10). Traditionally, the severity of chronic liver disease has been assessed using scoring systems such as the Child–Turcotte–Pugh (CTP) classification and the Model for End-Stage Liver Disease (MELD) score. Recognition of the prognostic value of serum sodium has led to the incorporation of serum sodium into the MELD-Na score, which has demonstrated improved prediction of mortality compared with the conventional MELD score alone (11). This highlights the importance of routine assessment of serum sodium as a simple, inexpensive, and readily available biochemical parameter that provides valuable prognostic information in patients with chronic liver disease (12). Despite increasing recognition of the clinical importance of hyponatremia, variations in serum sodium levels between compensated and decompensated chronic liver disease and their relationship with clinical outcomes remain inadequately characterized in many hospital settings, particularly in the Indian population (13). Early identification of patients at risk for hyponatremia may facilitate timely therapeutic interventions, optimize fluid and electrolyte management, improve monitoring strategies, and potentially reduce complications and mortality (14). Therefore, the present study aims to assess serum sodium levels in patients with compensated and decompensated chronic liver disease and evaluate their association with clinical outcomes. By comparing serum sodium concentrations across different stages of chronic liver disease and correlating them with disease severity and complications, this study seeks to determine the prognostic significance of serum sodium as an easily measurable biomarker that may aid in risk stratification and guide clinical decision-making in the management of patients with chronic liver disease. AIMS AND OBJECTIVES Aim • To assess serum sodium levels in patients with compensated and decompensated chronic liver disease and evaluate their association with clinical outcomes. Objective • To compare serum sodium levels between patients with compensated and decompensated chronic liver disease and determine their relationship with clinical outcomes.

This prospective observational study was conducted in the Department of General Medicine, Gadag Institute of Medical Sciences, Gadag, after obtaining approval from the Institutional Ethics Committee and written informed consent from all participants. The study was carried out over a period of July 2022 to July 2024. A total of 140 eligible adult patients with chronic liver disease were enrolled using purposive sampling, including 70 patients with compensated chronic liver disease (Group C) and 70 patients with decompensated chronic liver disease (Group D). Patients were categorized based on the presence or absence of complications such as ascites, hepatic encephalopathy, variceal bleeding, or jaundice. Patients with confirmed chronic liver disease who fulfilled the inclusion criteria were included in the study, whereas those with conditions likely to influence serum sodium levels independently of liver disease or those unwilling to participate were excluded. A detailed clinical history, demographic characteristics, etiology of chronic liver disease, comorbidities, alcohol consumption, and physical examination findings were recorded using a structured proforma. Baseline laboratory investigations included complete blood count, liver function tests, renal function tests, coagulation profile, and serum sodium estimation using the EASYLYTE Na/K analyser. Disease severity was assessed using the Model for End-Stage Liver Disease (MELD) score. Patients were evaluated for complications including ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome, hepatic hydrothorax, and variceal bleeding. Serum sodium levels were compared between compensated and decompensated chronic liver disease patients and correlated with disease severity, etiology, complications, and clinical outcomes. All patients were followed for six months to assess mortality and clinical outcomes. The collected data were entered into Microsoft Excel and analyzed using appropriate statistical software. Continuous variables were expressed as mean ± standard deviation, whereas categorical variables were presented as frequencies and percentages. Comparisons between the compensated and decompensated groups were performed using the independent Student's t-test for continuous variables and the Chi-square test or Fisher's exact test for categorical variables, as appropriate. A p value of <0.05 was considered statistically significant.

In the present study, the mean serum sodium level was 139.73 ± 4.49 mEq/L in patients with no ascites, 128.91 ± 1.83 mEq/L in patients with slight ascites, 130.02 ± 0.00 mEq/L in patients with slight to moderate ascites, 126.24 ± 2.49 mEq/L in patients with moderate gross ascites, and 124.11 ± 3.73 mEq/L in patients with gross ascites. The difference in mean serum sodium levels according to the severity of ascites was statistically significant (p<0.001). Table 8. Comparison of Mean Serum Sodium Levels According to Six-Month Mortality in Patients with Chronic Liver Disease Six-month mortality Serum Sodium (Mean ± SD) P value Yes 122.73 ± 4.02 No 134.71 ± 7.12 <0.001 In the present study, the mean serum sodium level was 122.73 ± 4.02 mEq/L among patients who died within six months and 134.71 ± 7.12 mEq/L among patients who survived at six months. The difference in mean serum sodium levels between patients with and without six-month mortality was statistically significant (p<0.001).

The present study assessed serum sodium levels in patients with compensated and decompensated chronic liver disease and evaluated their association with disease severity and clinical outcomes. The findings demonstrated significantly lower serum sodium levels in patients with decompensated chronic liver disease compared with compensated disease, with hyponatremia being associated with increased disease severity, greater ascites severity, and six-month mortality. In the present study, patients with decompensated chronic liver disease had significantly lower mean serum sodium levels than those with compensated disease (126.29 ± 3.99 vs. 139.70 ± 4.52 mEq/L; p<0.001). These findings are consistent with John and Thuluvath (2015), who described dilutional hyponatremia as a common consequence of advanced cirrhosis resulting from portal hypertension, splanchnic vasodilatation, and non-osmotic vasopressin release leading to impaired free water excretion (5). Similarly, Yadav et al. (2026) reported an association between lower serum sodium levels and adverse prognosis in patients with decompensated chronic liver disease (9). Rawat et al. (2026) also demonstrated a higher incidence of hyponatremia with increasing severity of chronic liver disease, supporting the present findings (13). The present study observed significantly higher MELD scores among patients with decompensated chronic liver disease, indicating more advanced hepatic dysfunction. This observation agrees with Acharya et al. (2019), who reported that MELD, Child–Turcotte–Pugh, and MELD-Na scores are valuable predictors of short-term mortality in end-stage liver disease, with the inclusion of serum sodium improving prognostic accuracy (11). Likewise, Prohic et al. (2016) demonstrated that lower serum sodium levels, even in patients with relatively low MELD scores, were associated with poor prognosis, emphasizing that hyponatremia provides prognostic information beyond conventional severity scoring systems (7). Alcoholic liver disease was the predominant etiology in the present study, particularly among patients with decompensated disease. This finding is in agreement with Sharma and Nagalli (2023), who identified alcohol-associated liver disease as one of the leading causes of chronic liver disease progression worldwide (1). Furthermore, Zhang et al. (2025) reported that although multiple etiologies contribute to the global burden of chronic liver disease, alcohol-related liver disease remains a major contributor to cirrhosis and liver-related mortality (3). Kumar et al. (2023) also emphasized that persistent etiological injury, particularly alcohol consumption, accelerates the transition from compensated to decompensated cirrhosis (4). The present study demonstrated significantly higher frequencies of ascites, hydrothorax, hepatorenal syndrome, spontaneous bacterial peritonitis, hepatic encephalopathy, variceal bleeding, and six-month mortality among decompensated patients. These observations correspond well with the pathophysiological mechanisms described by Engelmann et al. (2021), who reported that portal hypertension, systemic inflammation, circulatory dysfunction, and metabolic disturbances contribute to progressive hepatic decompensation and its complications (2). Oliver et al. (2025) similarly described portal hypertension as the central mechanism underlying the development of ascites, variceal bleeding, and other complications of advanced liver disease (6). An important finding of the present study was the significant association between lower serum sodium levels and increasing severity of ascites as well as six-month mortality. Patients who died during follow-up had markedly lower serum sodium levels than survivors. These findings closely resemble those reported by Jenq et al. (2010), who demonstrated that serum sodium independently predicts mortality among critically ill cirrhotic patients (12). Likewise, Prohic et al. (2016) showed that hyponatremia and ascites were strong predictors of adverse outcomes even among patients with relatively low MELD scores (7). Yadav et al. (2026) reported an association between lower serum sodium and adverse prognosis marker in decompensated chronic liver disease (9). The neurological implications of hyponatremia observed in patients with hepatic encephalopathy are supported by Fujisawa et al. (2016), who demonstrated that chronic hyponatremia contributes to neurological and cognitive impairment (8). Chawla et al. (2026) also emphasized that prompt recognition and correction of clinically significant hyponatremia are important to reduce neurological complications and improve patient outcomes (14). Overall, the findings of the present study are consistent with the available literature and demonstrate that serum sodium is a simple, inexpensive, and readily available biomarker that reflects disease severity and is significantly associated with greater ascites severity and six-month mortality in patients with chronic liver disease. Routine assessment of serum sodium, together with established prognostic scores, may improve risk stratification, facilitate early identification of high-risk patients, and support timely therapeutic interventions.

The present study demonstrated that serum sodium levels were significantly lower in patients with decompensated chronic liver disease compared with those having compensated disease. Hyponatremia was associated with greater disease severity, as reflected by higher MELD scores and abnormal liver function parameters. Decompensated patients had a significantly higher frequency of complications, including ascites, hydrothorax, hepatorenal syndrome, spontaneous bacterial peritonitis, hepatic encephalopathy, and variceal bleeding, while lower serum sodium levels were significantly associated with greater ascites severity and increased six-month mortality. Alcoholic liver disease was the predominant etiology, particularly among patients with decompensated disease. These findings suggest that serum sodium is a simple, inexpensive, and readily available biochemical marker that can aid in the assessment of disease severity, risk stratification, and prediction of adverse clinical outcomes in patients with chronic liver disease. Routine monitoring of serum sodium may facilitate early identification of high-risk patients and support timely therapeutic interventions to improve overall clinical outcomes.

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