MAFLD and glomerular hyperfiltration in subjects with normoglycemia, prediabetes and type 2 diabetes: A cross‐sectional population study

Abstract

AbstractBackgroundMetabolic dysfunction‐associated fatty liver disease (MAFLD, 2020 diagnostic criteria) and glomerular hyperfiltration share common risk factors, including obesity, insulin resistance, impaired glucose tolerance, diabetes, dyslipidemia, and hypertension.AimsTo assess the prevalence of MAFLD and its association with glomerular hyperfiltration and age‐related worsening of kidney function in subjects with normoglycemia, prediabetes and type 2 diabetes mellitus (T2DM).MethodsWe analysed data recorded during occupational health visits of 125,070 Spanish civil servants aged 18–65 years with a de‐indexed glomerular filtration rate (GFR) estimated with the chronic‐kidney‐disease‐epidemiological (CKD‐EPI) equation (estimated glomerular filtration rate [eGFR]) ≥60 mL/min. Subjects were categorised according to fasting plasma glucose levels <100 mg/dL (normoglycemia), ≥100 and ≤ 125 mg/dL (prediabetes), or ≥126 mg/dL and/or antidiabetic treatment (T2DM). The association between MAFLD and glomerular hyperfiltration, defined as a de‐indexed eGFR above the age‐ and gender‐specific 95th percentile, was assessed by multivariable logistic regression.ResultsIn the whole study group, MAFLD prevalence averaged 19.3%. The prevalence progressively increased from 14.7% to 33.2% and to 48.9% in subjects with normoglycemia, prediabetes and T2DM, respectively (p < 0.001 for trend). Adjusted odds ratio (95% CI) for the association between MAFLD and hyperfiltration was 9.06 (8.53–9.62) in the study group considered as a whole, and 8.60 (8.03–9.21), 9.52 (8.11–11.18) and 8.31 (6.70–10.30) in subjects with normoglycemia, prediabetes and T2DM considered separately. In stratified analyses, MAFLD amplified age‐dependent eGFR decline in all groups (p < 0.001).ConclusionsMAFLD prevalence increases across the glycaemic spectrum. MAFLD is significantly associated with hyperfiltration and amplifies the age‐related eGFR decline.