# Uric acid-to-albumin ratio as a cardiometabolic marker for predicting adverse outcomes in patients with atrial fibrillation: evidence from two independent cohorts

**Authors:** Aobo Gong, Ying Cao, Zexi Li, Fanghui Li, Wenjie Li, Bangjiaxin Ren, Xianjin Hu, Yifan Zhou, Rui Zeng

PMC · DOI: 10.3389/fendo.2026.1786997 · Frontiers in Endocrinology · 2026-02-13

## TL;DR

This study shows that the uric acid-to-albumin ratio (UAR) is a useful predictor of mortality in patients with atrial fibrillation, beyond traditional risk scores.

## Contribution

The study demonstrates that UAR provides incremental prognostic value over existing risk scores for predicting mortality in atrial fibrillation patients.

## Key findings

- Higher UAR is independently associated with increased 1-year all-cause mortality in atrial fibrillation patients.
- Adding UAR to the CHA2DS2-VASc score improves risk prediction accuracy and reclassification.
- SHAP analysis confirms UAR as a major contributor to mortality prediction in both cohorts.

## Abstract

Atrial fibrillation (AF) is closely associated with metabolic dysfunction. The uric acid–to–albumin ratio (UAR), integrating oxidative stress, inflammation, and nutritional status, reflect cardiometabolic burden, but evidence linking UAR to AF prognosis remains limited.

We analyzed clinical data from 1,908 AF patients at West China Hospital, with external validation from the MIMIC database (n=1,366). Associations were assessed using Kaplan–Meier analyses, restricted cubic splines, and multivariable Cox proportional hazards models. Incremental prognostic value beyond the CHA2DS2-VASc score was evaluated in both cohorts. Exploratory machine learning and SHAP analyses were employed to assess the variable importance of UAR. Subgroup and sensitivity analyses were performed in primary cohort, including additional cardiometabolic adjustment, analyses with cardiac mortality, competing risk models, and longer follow-up.

Baseline characteristics differed across UAR quartiles, with high UARs associated with substantial burdens of metabolic comorbidities, heart failure, renal dysfunction, and elevated inflammatory and cardiac biomarkers. Mortality was higher in the highest UAR quartile (log-rank P<0.001). In the primary cohort, restricted cubic splines showed a J-shaped association between UAR and 1-year mortality (P for nonlinearity <0.001). In fully adjusted Cox models, UAR (per SD) predicted 1-year all-cause mortality in the primary cohort (HR 1.162, 95% CI 1.036–1.304) and in the MIMIC cohort (HR 1.137, 95% CI 1.092–1.185). Adding UAR to the CHA2DS2-VASc score improved discrimination (C-index 0.654 to 0.692; P = 0.001), reclassification (continuous NRI 0.178), calibration, and clinical net benefit, with consistent incremental performance in the MIMIC cohort. In both cohorts, SHAP analysis consistently identified UAR as one of the major contributors to mortality prediction. Findings were consistent across subgroups and sensitivity analyses.

UAR is an independent predictor of mortality in AF and captures cardiometabolic remodeling beyond conventional risk assessment. As a readily available biomarker, UAR may facilitate metabolically guided risk stratification and individualized management in AF populations.

## Linked entities

- **Diseases:** atrial fibrillation (MONDO:0004981), heart failure (MONDO:0005252)

## Full-text entities

- **Genes:** TNNT2 (troponin T2, cardiac type) [NCBI Gene 7139] {aka CMD1D, CMH2, CMPD2, LVNC6, RCM3, TnTC}, ITIH2 (inter-alpha-trypsin inhibitor heavy chain 2) [NCBI Gene 3698] {aka H2P, ITI-HC2, SHAP}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, GGTLC5P (gamma-glutamyltransferase light chain 5 pseudogene) [NCBI Gene 653590] {aka GGT}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318] {aka CLG4B, GELB, MANDP2, MMP-9}, KCNA5 (potassium voltage-gated channel subfamily A member 5) [NCBI Gene 3741] {aka ATFB7, HCK1, HK2, HPCN1, KV1.5, PCN1}, GGT1 (gamma-glutamyltransferase 1) [NCBI Gene 2678] {aka CD224, D22S672, D22S732, GGT, GGT 1, GGTD}, CMPK1 (cytidine/uridine monophosphate kinase 1) [NCBI Gene 51727] {aka CK, CMK, CMPK, UMK, UMP-CMPK, UMPK}
- **Diseases:** MIMIC-III (MESH:C000657744), DM (MESH:D003920), endothelial dysfunction (MESH:D014652), atrial fibrotic remodeling (MESH:D064752), Chronic inflammation (MESH:D007249), critically ill (MESH:D016638), hyperglycemia (MESH:D006943), frailty (MESH:D000073496), impaired nutritional status (MESH:D009748), metabolic (MESH:D008659), COPD (MESH:D029424), atrial cardiomyopathy (MESH:D009202), stroke (MESH:D020521), cardiac arrhythmia (MESH:D001145), insulin resistance (MESH:D007333), cardiovascular death (MESH:D002318), AF (MESH:D001281), Mortality (MESH:D003643), malnutrition (MESH:D044342), HT (MESH:D006973), CAD (MESH:D003324), TIA (MESH:D002546), peripheral arterial disease (MESH:D058729), obstructive sleep apnea syndrome (MESH:D020181), systemic embolism (MESH:D004617), impaired renal function (MESH:D007674), HF (MESH:D006333)
- **Chemicals:** triglyceride (MESH:D014280), bilirubin (MESH:D001663), UA (MESH:D014527), ACEI (-), glucose (MESH:D005947), creatinine (MESH:D003404), reactive oxygen species (MESH:D017382), lipid (MESH:D008055)
- **Species:** Homo sapiens (human, species) [taxon 9606]

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## References

39 references — full list in the complete paper: https://tomesphere.com/paper/PMC12945761/full.md

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Source: https://tomesphere.com/paper/PMC12945761