Is metabolic‐dysfunction‐associated fatty liver disease or advanced liver fibrosis associated with erythropoietin stimulating agent hypo‐responsiveness among patients with end‐stage kidney disease on haemodialysis?

Abstract

AbstractAimThis study aims to determine if metabolic‐dysfunction‐associated fatty liver disease (MAFLD) or advanced liver fibrosis is associated with erythropoietin stimulating agent (ESA) hypo‐responsiveness in hemodialysis patients.MethodsIn a cross‐sectional study of 379 hemodialysis patients, FibroTouch transient elastography was performed on all patients. Erythropoeitin resistance index (ERI) was used to measure the responsiveness to ESA. Patients in the highest tertile of ERI were considered as having ESA hypo‐responsiveness.ResultsThe percentage of patients with ESA hypo‐responsiveness who had MAFLD was lower than patients without ESA hypo‐responsiveness. FIB‐4 index was significantly higher in ESA hypo‐responsive patients. In multivariate analysis, female gender (aOR = 3.4, 95% CI = 1.9–6.2, p < 0.001), dialysis duration ≥50 months (aOR = 1.8, 95% CI = 1.1–2.9, p < 0.05), elevated waist circumference (aOR = 0.4, 95% CI = 0.2–0.8, p = 0.005), low platelet (aOR = 2.6, 95% CI 1.3–5.1, p < 0.01), elevated total cholesterol (aOR = 0.5, 95% CI 0.3–0.9, p < 0.05) and low serum iron (aOR = 3.8, 95% CI = 2.3–6.5, p < 0.001) were found to be independent factors associated with ESA hypo–responsiveness. Neither MAFLD nor advanced liver fibrosis was independently associated with ESA hypo–responsiveness. However, every 1 kPA increase in LSM increased the chance of ESA–hyporesponsiveness by 13% (aOR = 1.1, 95% CI =  1.0–1.2, p = 0.002) when UAP and LSM were used instead of presence of MAFLD and advanced liver fibrosis, respectively.ConclusionMAFLD and advanced liver fibrosis were not independently associated with ESA hypo‐responsiveness. Nevertheless, higher FIB‐4 score in ESA hypo‐responsive group and significant association between LSM and ESA hypo‐responsiveness suggest that liver fibrosis may be a potential clinical marker of ESA hypo‐responsiveness.