Exploring Biomarkers for Metabolic Complications in NAFLD: The Uric Acid-to-Creatinine Ratio

According to a recent study, uric acid-to-creatinine ratio (SUA/Cr) identifies metabolic risk and may support screening and risk stratification in patients with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes.

The primary cross-sectional study linked higher SUA/Cr to an adverse metabolic profile—higher total and LDL cholesterol, raised alanine aminotransferase, and greater central adiposity—suggesting a low-cost, noninvasive marker for earlier risk detection. Because the ratio adjusts uric acid for creatinine (a proxy for renal function), it helps contextualize hyperuricemia within routine metabolic assessment and could be actionable in primary diabetes care.

In a cross-sectional cohort of 226 adults with ultrasonography‑confirmed disease, investigators examined lipid measures, liver enzymes and measures of central adiposity as primary endpoints and found consistent associations across these domains. Total cholesterol rose from ~174 to ~192 mg/dL and LDL‑C from ~97 to ~131 mg/dL across increasing SUA/Cr tertiles; alanine aminotransferase was higher in the upper tertiles and waist circumference increased from about 100 to 104 cm.

Triglycerides and HDL did not differ significantly, and BMI was similar across groups while waist measures and waist‑to‑hip ratio tracked with the ratio—pointing to abdominal adiposity as the dominant anthropometric correlate. These directions support SUA/Cr as a metabolic risk correlate rather than evidence of a causal driver of liver injury.

Elevated SUA/Cr in people with NAFLD and diabetes may flag patients at higher metabolic risk. Biologically, a higher uric acid relative to creatinine may reflect insulin resistance, lipotoxicity and hepatic oxidative stress pathways that associate with dyslipidemia and mild hepatocellular injury, but these links remain inferential. Key limitations temper interpretation: the design was cross‑sectional, sampling was single‑center, and the cohort excluded advanced steatosis—so causality and broad generalizability are unproven. Longitudinal, multicenter validation is required to confirm predictive value for liver-disease progression.

Clinicians can calculate SUA/Cr from routine labs (serum uric acid ÷ serum creatinine) at baseline and during annual metabolic reviews for patients with type 2 diabetes and suspected or confirmed NAFLD—especially those with central obesity or atherogenic lipids. The incremental cost is negligible when both analytes are already measured, and the ratio is easy to compute in an electronic medical record or by hand. An elevated SUA/Cr alongside adverse lipids or raised ALT can prompt stepped-up lifestyle counseling, earlier lipid optimization, and consideration of hepatology referral when multiple risk signals co‑occur—framing SUA/Cr as a low‑burden augmentation to existing screening workflows.