Answers are grounded in this paper and cite their sources.
This investigation identifies IL-18, KIM-1, and FGF-23 for early AKI prediction in cirrhotic patients, suggesting enhanced risk assessment.
Acute kidney injury (AKI) is a potentially fatal complication in patients with decompensated cirrhosis having therapeutic paracentesis, and early diagnosis is still difficult because of the low sensitivity of serum creatinine. We preemptively tested serum interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1), and fibroblast growth factor-23 (FGF-23) in early prediction of post-paracentesis AKI in 80 hospitalized patients with tense ascites and normal baseline kidney function. Samples of blood were collected 2 h pre-paracentesis and 24 h post-paracentesis. Based on the Kidney Disease: Improving Global Outcomes definition, AKI, which happened within 72 h, was present in 40% of patients. Biomarkers levels at baseline were comparable. In 24 h of paracentesis, IL-18, KIM-1, and FGF-23 were high in patients who later developed AKI (all p value below .001) and had high-absolute changes than the non-AKI group. The largest discriminative performance was observed of FGF-23 (area under the curve 0.959), then IL-18 (0.931), and KIM-1 (0.903). In multivariate logistic regression controlling MELD-Na score, serum albumin, baseline eGFR and ascitic fluid volume, the post-paracentesis FGF-23 was still independently connected with AKI. Biomarkers of tubular injury, especially FGF-23, which increased shortly after the procedure were strongly correlated with future AKI and could increase risk stratification pending external validation.
No takes yet. Share an insight, caveat, or question.
Fayed et al. (2026) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: