A recent study linking serum uric acid to diabetes risk in coronary heart disease patients faces scrutiny over potential confounders, highlighting the need for standardised methods and detailed medication data before confirming causation.
A letter to the editor has urged caution over a 2026 multicentre cohort study in Diabetes, Metabolic Syndrome and Obesity that linked higher serum uric acid to a greater risk of new-onset diabetes in people with coronary heart disease. In the study, Shuaiwei Song and colleagues reported a non-linear association, sex-specific risk thresholds, and partial mediation by inflammatory markers, with inflammation explaining as much as 32.27% of the observed effect. The authors also said SUA added some predictive value for diabetes risk in this high-risk group. (pmc.ncbi.nlm.nih.gov)
The letter argues that the analysis may not have fully accounted for kidney function, a key issue because uric acid levels and renal performance are closely linked. In the original paper, patients with severe renal dysfunction were excluded, but the commentary says milder impairment was not separately adjusted for or tested in subgroups. That concern is supported by wider literature: a Brazilian study in people with type 1 diabetes found higher SUA was inversely associated with glomerular filtration rate, while another large diabetes cohort linked higher SUA to worse mortality outcomes, underscoring how kidney function can shape interpretation of uric-acid data. (pmc.ncbi.nlm.nih.gov)
The letter also points to the need for clearer standardisation across the five participating hospitals. Song’s team said blood samples were collected using standard procedures and analysed on fully automated biochemical analysers, but the commentary notes that the study does not spell out whether the centres used identical assay methods or whether calibration across sites was checked. That matters because even small laboratory differences can affect serum uric acid comparisons, and the multicentre design means any regional variation in diet, access to care or testing practice could influence the findings. (pmc.ncbi.nlm.nih.gov)
Two other concerns relate to medication history and outcome definition. The study excluded people taking several uric-acid-lowering or uric-acid-altering drugs at baseline, including febuxostat, benzbromarone, allopurinol and diuretics, but the letter says it is unclear whether a sufficient washout period was required or whether other agents that can affect uric acid, such as aspirin or ciclosporin, were considered. It also says the diabetes endpoint should have been described more explicitly in the methods. The paper states that new-onset diabetes was diagnosed using accepted clinical criteria, including symptoms with elevated random glucose, fasting glucose, oral glucose tolerance testing or HbA1c of at least 6.5%, but the letter argues that the study would have been stronger with sensitivity analyses based on different diagnostic approaches. (pmc.ncbi.nlm.nih.gov)
Even so, the study adds to a growing body of evidence that elevated serum uric acid may track with metabolic and cardiovascular risk, particularly in patients already living with coronary disease. Other recent and older studies have also linked uric acid with coronary disease, inflammation, renal decline and later diabetes, suggesting the marker may deserve closer attention. The broader message from the commentary is not that the association is unimportant, but that future work should measure kidney function more fully, harmonise laboratory methods across centres and record medication history in greater detail before drawing firm conclusions about causation. (pmc.ncbi.nlm.nih.gov)
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