DOI: 10.4103/wkbj.wkbj_12_26 ISSN: 3118-0132

Association between Serum Albumin Levels and the Frequency of Ascites Development in Patients with Liver Cirrhosis: A Retrospective Analysis

Akzhan M. Madenbayeva, Yerlan Sh. Bazargaliyev, Sagyndyk S. Rysmaganbetov, Saima Khan, Arailym Ye. Izturganova, Aygerim K. Issayeva
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BSTRACT

Background:

Ascites is the most common complication of liver cirrhosis and represents a hallmark of hepatic decompensation. Although hypoalbuminemia has traditionally been considered a key contributor to ascites formation through reduced plasma oncotic pressure, its independent association with ascites severity remains controversial.

Aim:

The aim of this study was to evaluate the relationship between serum albumin levels and the presence and severity of ascites in patients with liver cirrhosis and to determine whether albumin may serve as a reliable marker of hepatic decompensation.

Materials and Methods:

A retrospective analytical study was conducted, including 95 adult patients with confirmed liver cirrhosis hospitalized between January 2023 and December 2024. Clinical, laboratory, and imaging data were extracted from medical records. Ascites severity was classified into four stages (0–3). Serum albumin levels were compared across ascites stages using non-parametric tests. Spearman correlation and logistic regression analyses were performed to assess the independent association between serum albumin and ascites severity.

Results:

The mean serum albumin concentration was 30.6 ± 7.1 g/L. Albumin levels progressively declined with increasing ascites severity, from 36.1 ± 6.7 g/L in patients without ascites to 28.1 ± 6.0 g/L in those with stage 3 ascites. A significant negative correlation was observed between albumin level and ascites stage ( r s = −0.29, P = 0.007). Kruskal–Wallis analysis demonstrated significant differences among the groups ( P < 0.05). Post hoc testing revealed significantly lower albumin levels in stage 3 compared with stages 0 and 1 (adjusted P = 0.025). In logistic regression models, serum albumin independently predicted advanced ascites (odds ratio [OR] = 0.88; 95% confidence interval [CI]: 0.79–0.97; P = 0.016). Ordinal regression confirmed that each 1 g/L increase in albumin was associated with a 9% reduction in the odds of higher ascites severity (OR = 0.91; 95% CI: 0.86–0.96).

Conclusion:

Lower serum albumin levels are independently associated with greater ascites severity in liver cirrhosis. Although albumin does not fully explain ascites development, it serves as a clinically relevant marker of advanced hepatic decompensation and may contribute to improved risk stratification.

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