Background: Hyponatremia is a common and clinically significant complication in patients with chronic liver disease (CLD), often associated with increased morbidity and progression to hepatic decompensation. While its prevalence in hospitalized cirrhotic patients is well documented, data from outpatient populations remain limited. Objective: Therefore, the aim of our study was to determine the frequency of hyponatremia in patients with CLD presenting to the outpatient department. Methods: This cross-sectional study was conducted at the outpatient department of Medical Unit V, Jinnah Sindh Medical University, between January and December 2019. A total of 224 patients with clinically and/or radiologically diagnosed CLD were included using non-probability consecutive sampling. Patients with conditions or medications known to cause hyponatremia were excluded. Serum sodium levels were used to classify hyponatremia as mild (130-134 mmol/L), moderate (125-129 mmol/L), and severe (<125 mmol/L). Data on demographic, clinical, and laboratory parameters were collected and analyzed using IBM SPSS Statistics for Windows, Version 27 (Released 2019; IBM Corp., Armonk, New York, United States). Results: Out of 224 patients, 94 (42%) were found to have hyponatremia, with 52 (23.2%) having mild hyponatremia, 29 (12.9%) moderate hyponatremia, and 13 (5.8%) severe hyponatremia. The most common cause of CLD was hepatitis C (34.8%), followed by hepatitis B (27.2%) and metabolic associated fatty liver disease (17.4%). Hyponatremia was significantly associated with lower hemoglobin and serum albumin levels, presence of ascites, and elevated INR, total bilirubin, Child-Turcotte-Pugh (CTP) score, and model for end-stage liver disease score (p<0.05 for all), indicating more advanced liver disease. Conclusion: Hyponatremia is prevalent in stable CLD patients presenting to outpatient clinics and correlates strongly with indicators of disease severity. Routine monitoring of serum sodium levels in outpatient settings may enable early identification of high-risk individuals and timely therapeutic interventions to delay hepatic decompensation.
Bajkani et al. (Sun,) studied this question.