Key result
Higher uric acid-to-albumin ratio linked to ~24% higher mortality per SD in dilated cardiomyopathy.
Why the study?
Nutritional and metabolic abnormalities may contribute to adverse outcomes in dilated cardiomyopathy, and the prognostic value of the uric acid-to-albumin ratio (UAR) in this context was unclear.
Does an elevated uric acid-to-albumin ratio (UAR) predict increased all-cause mortality in patients with dilated cardiomyopathy?
Cohort (n=445)
No
Does an elevated uric acid-to-albumin ratio (UAR) predict increased all-cause mortality in patients with dilated cardiomyopathy?
Hazard Ratio: 1.24 (95% CI 1.03–1.5)
p-value: p=0.025
A higher uric acid-to-albumin ratio is independently associated with increased all-cause mortality in patients with dilated cardiomyopathy, though it does not significantly improve risk prediction when added to established clinical covariates and NT-proBNP.
UAR should not yet inform risk stratification in dilated cardiomyopathy; leaves open whether this metabolic marker warrants prospective validation.
Background Nutritional and metabolic abnormalities may contribute to adverse outcomes in dilated cardiomyopathy (DCM). The uric acid-to-albumin ratio (UAR), derived from two routinely measured biochemical parameters, may reflect this broader systemic burden. This study examined whether UAR was related to all-cause mortality and prognostic risk stratification in patients with DCM. Methods The analysis included 445 patients with DCM. UAR was derived from baseline serum uric acid and albumin measurements and was evaluated as a standardized continuous measure, quartile-based categories, and a dichotomous variable. Multivariable Cox regression models were applied to estimate the relationship between UAR and all-cause mortality. Restricted cubic splines were used to characterize the shape of the association between UAR and mortality, while subgroup analyses, sensitivity analyses, N-terminal pro-B-type natriuretic peptide (NT-proBNP)-based joint stratification, and prediction metrics were performed to assess consistency, robustness, and incremental prognostic value. Results At a median observation time of 771 days, 135 patients had died. Patients with higher UAR generally showed greater cardiac biomarker elevation, higher renal biochemical burden, lower albumin concentrations, and a greater proportion of deaths. After full adjustment for demographic characteristics, comorbidities, cardiac status, renal function, and ln(NT-proBNP), UAR remained related to all-cause mortality when modeled per 1-SD increment (HR of 1.24; 95% CI from 1.03 to 1.50). When the lowest quartile was used as the reference, elevated UAR was also linked to a higher mortality risk (HR of 2.50; 95% CI from 1.47 to 4.26). Quartile-specific hazard ratios were non-monotonic. Spline modeling supported an overall association between UAR and mortality (P for overall = 0.018), while the test for nonlinearity did not reach statistical significance (P for nonlinearity = 0.076). In the joint analysis, the subgroup with both elevated UAR and high NT-proBNP had the greatest risk of death (HR of 4.30; 95% CI from 2.16 to 8.58). When UAR was added to a model containing clinical covariates and ln(NT-proBNP), no incremental improvement in prognostic performance was demonstrated (ΔC-index = 0.0074; 95% CI, − 0.0023 to 0.0162; P = 0.272), and neither IDI nor category-free NRI indicated improvement. Conclusion Higher UAR was associated with poorer survival in patients with DCM. However, adding UAR to a model containing established clinical variables and ln(NT-proBNP) did not demonstrate incremental improvement in prognostic performance. Clinical trial number Not applicable.
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Tian et al. (2026) conducted a cohort in Dilated cardiomyopathy (n=445). Uric acid-to-albumin ratio (UAR) vs. Lower UAR (analyzed per 1-SD increment or lowest quartile) was evaluated on All-cause mortality (HR 1.24, 95% CI 1.03-1.50, p=0.025). Higher uric acid-to-albumin ratio was independently associated with an increased risk of all-cause mortality in patients with dilated cardiomyopathy (HR 1.24 per 1-SD increment).
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