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Finds higher FIB-4 and prediabetes predict eGFR decline in nondiabetic adults, suggesting a metabolic link to renal risk.
Introduction and Objective: Metabolic dysfunction-associated steatotic liver disease (MASLD) has been linked to chronic kidney disease (CKD), with fibrosis as the potential pathogenic factor shared by both diseases. The Fibrosis-4 (FIB-4) index is a widely used non-invasive fibrosis marker; however, its association with renal outcomes remains uncertain. We evaluated the relationship between FIB-4, estimated glomerular filtration rate (eGFR) decline and albuminuria in the ILERVAS cohort. Methods: We included 3,940 adults aged 45-70 years from the ILERVAS study, all free of diabetes, CKD and chronic liver disease. FIB-4 was analysed categorically (<1.30 vs. ≥1.30) and continuously in regression models. Renal outcomes were eGFR and albuminuria (albumin-to-creatinine ratio ≥30 mg/g) at baseline and 4 years. Multivariable linear and logistic regression models were adjusted for age, sex, hypertension, presence of prediabetes, adiposity, lipids and smoking. Results: At baseline, 78.3% of participants were classified as low FIB-4 risk and 21.7% as indeterminate-high risk; the latter were older and had lower eGFR, whereas albuminuria prevalence was similar. At 4 years (n=1,593), eGFR remained lower in the indeterminate-high group, with no differences in albuminuria prevalence. In multivariable analyses, higher FIB-4 values and prediabetes independently predicted greater eGFR decline (β =−1.15 and -1.57; p=0.013 and 0.023, respectively). Age, female sex, baseline eGFR and hypertension also emerged as independent predictors of eGFR decline. Conclusion: In adults at low-to-moderate cardiovascular risk without diabetes or established liver/kidney disease, both higher FIB-4 values and prediabetes were independently associated with faster eGFR loss. FIB-4 may help to capture systemic metabolic factors related to fibrosis, suggesting its potential role in renal risk stratification. Disclosure A. Lecube: None. J.L. Mengíbar: None. R. Simo: Research Support; Current; Abbott, Dexcom, Inc., Novo Nordisk. Board Member; Current; D-Sight. C. Hernández: None. O. Simó-Servat: Advisory Panel; Current; Abbott Diabetes. Other - Speaker on a meeting; Ended; Tandem Diabetes Care, Inc. P. Gil-Millán: None. Á. Ortiz Zúñiga: None. A. Switzer-Rodriguez: None. Funding This research was supported by grants from the Diputació de Lleida.
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