ArticleCureus2026
Role of the Hepatorenal Index in the Detection of HbA1c-Defined Dysglycemia in Patients With Non-alcoholic Fatty Liver Disease: A Cross-Sectional Study.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background Non-alcoholic fatty liver disease (NAFLD), increasingly discussed within the metabolic dysfunction-associated steatotic liver disease (MASLD) framework, is closely linked to insulin resistance and abnormal glucose metabolism. The hepatorenal index (HRI) provides a quantitative ultrasound estimate of hepatic steatosis, but its value for detecting HbA1c-defined dysglycemia remains uncertain. Objective The primary objective was to estimate the prevalence of HbA1c-defined dysglycemia among adults with ultrasonographically diagnosed NAFLD. Secondary objectives were to assess the association between HRI and HbA1c and to evaluate the independent association and discriminatory performance of HRI for dysglycemia. Methods This cross-sectional study included 116 adults with NAFLD evaluated at Government Medical College Manjeri, India, from August 2025 to February 2026. HRI was calculated from standardized B-mode ultrasound images using liver-to-right renal cortical echogenicity ratios, and the mean of three paired measurements was used for analysis. Dysglycemia was defined as HbA1c ≥5.7%, comprising prediabetes-range HbA1c (5.7-6.4%) and diabetes-range HbA1c (≥6.5%). Pearson and Spearman correlations, linear and robust regression, logistic regression, and receiver operating characteristic (ROC) analyses were performed. Results HbA1c-defined dysglycemia was present in 69 of 116 participants (59.5%), including 36 (31.0%) with prediabetes-range HbA1c and 33 (28.4%) with diabetes-range HbA1c. Mean HRI was 1.54 (SD 0.28). HRI showed a weak positive Pearson correlation with HbA1c (r = 0.232; p = 0.012), whereas Spearman correlation was not significant (rho = 0.111; p = 0.237). The association was attenuated in Huber robust regression and was not statistically significant after adjustment for age, sex, and body mass index (BMI) (beta = 0.41; 95% CI -0.19 to 1.01; p = 0.180). HRI was not independently associated with HbA1c-defined dysglycemia in adjusted logistic regression (OR per 0.1-unit increase = 1.05; 95% CI 0.91 to 1.21; p = 0.501). ROC analysis showed poor standalone discrimination (AUC = 0.547; 95% CI 0.433 to 0.653; p = 0.393). The sample-derived Youden threshold of HRI ≥1.71 had a sensitivity of 40.6% and specificity of 78.7% and was considered exploratory. Conclusion HRI showed at most a weak, method-sensitive association with HbA1c and poor standalone discrimination for HbA1c-defined dysglycemia. HRI may support sonographic quantification of hepatic steatosis but should not replace direct biochemical screening for dysglycemia.
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