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Table · dataset · 2026

Data Sheet 1_Serum uric acid variability and short-term mortality in chronic kidney disease: a retrospective cohort study with independent replication in MIMIC-IV.docx

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Inroduction<p>Within-person variation in serum uric acid (SUA) may reflect clinical instability, but its association with outcomes in chronic kidney disease (CKD) is uncertain.</p>Methods<p>We studied 10,556 adults with EHR-defined CKD and at least three SUA measurements during a 365-day baseline window across a nine-hospital consortium. Variability was quantified primarily by the coefficient of variation (CV); the primary outcome was all-cause mortality, and secondary outcomes were a composite kidney endpoint and major adverse cardiovascular events (MACE).

Cox models adjusted for demographics, comorbidities, baseline laboratory values, mean SUA, measurement number and medication use. Reproducibility of the short-term mortality association was assessed in MIMIC-IV.</p>Results<p>During a median follow-up of 0.62 years, 649 deaths, 676 kidney events and 3,172 first MACE occurred. Higher SUA CV was associated with mortality in the fully adjusted model (hazard ratio [HR] per 1-SD increase 1.24, 95% CI 1.15–1.32; highest versus lowest tertile 1.87, 95% CI 1.50–2.33), whereas adjusted associations with kidney events (HR 1.01, 95% CI 0.93–1.10) and MACE (HR 1.02, 95% CI 0.98–1.05) were null.

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Of all deaths, 495 (76.3%) occurred within 90 days. In a post-90-day landmark analysis of 6,784 participants with more than 90 days of follow-up, the mortality association was not observed (154 deaths; HR 1.02, 95% CI 0.86–1.21). Results were similar after daily aggregation of SUA measurements and additional adjustment for urate-lowering therapy, colchicine and sodium-glucose cotransporter-2 inhibitors.

In MIMIC-IV (n = 5,350; 931 deaths within 90 days), the adjusted HR per 1-SD increase in CV was 1.32 (95% CI 1.26–1.38).</p>Discussion<p>Greater SUA variability was associated with mortality during short follow-up; the concentration of deaths within 90 days and the null post-90-day landmark estimate suggest that the exposure may primarily mark near-term clinical deterioration rather than a causal or durable long-term prognostic mechanism.</p>

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