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Published on: March 24, 2023
Associations Between Urinary Metabolic Indicators and Metabolic Dysfunction-Associated Steatotic Liver Disease and
Jiacheng Cai1, Hong Wang1, Leilei Wang1
1The Third People's Hospital of Yinzhou District, Zhejiang, People's Republic of China.
Background/Aims:
Metabolic dysfunction-associated steatotic liver disease (MASLD) reflects the central role of systemic metabolic disturbances in the pathogenesis of fatty liver. Urinary metabolic indicators may capture integrated renal, inflammatory, and metabolic alterations associated with MASLD and liver fibrosis.
Materials And Methods:
The authors analyzed 3496 adults from the 2017-2020 National Health and Nutrition Examination Survey cycles. Urinary metabolic indicators-including serum uric acid-to-creatinine ratio (SUACR), urinary albumin-to-creatinine ratio (UACR), uric acid-to-high-density lipoprotein cholesterol ratio (UHR), uric acid-to-albumin ratio (UAR), and blood urea nitrogen-to-creatinine ratio (BUN/Cr)-were assessed. MASLD and liver fibrosis were defined using controlled attenuation parameter (CAP) and liver stiffness measurement (LSM), respectively. Associations were evaluated using multivariable regression models adjusted for demographic, lifestyle, and cardiometabolic factors.
Results:
Higher SUACR, UACR, UHR, and UAR were positively associated with CAP and MASLD (all P < .05), whereas BUN/Cr was not significantly associated with either outcome. For liver fibrosis, SUACR, UHR, and UAR remained independently associated after multivariable adjustment. Nonlinear, threshold-dependent patterns were observed for SUACR, UHR, and UAR with MASLD and for UHR with fibrosis. Among the urinary metabolic indicators, UHR demonstrated the strongest predictive performance for MASLD, whereas UACR demonstrated the best predictive performance for fibrosis.
Conclusion:
Urinary metabolic indicators, particularly uric acid-related indicators, were associated with MASLD and liver fibrosis, suggesting that they may reflect systemic metabolic and renal dysregulation. These findings support their potential utility for noninvasive risk assessment and warrant further investigation into their mechanistic role in the progression of fatty liver disease.
