Clinica chimica acta; international journal of clinical chemistry · 2026
Soluble suppression of tumorigenicity 2 and cardiovascular outcomes across serum uric acid strata in maintenance hemodialysis: an exploratory secondary analysis.
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Su Yiqi, Zhang Zhen, Lin Liyu, Teng Jie, Ding Xiaoqiang, Zou Jianzhou
Аннотация
BACKGROUND: In maintenance hemodialysis (MHD), serum uric acid (UA) is influenced by nutritional, inflammatory, and dialysis-related factors. Whether the prognostic association of soluble suppression of tumorigenicity 2 (sST2) differs according to UA remains uncertain.
METHODS: This retrospective secondary analysis included 358 MHD patients with baseline UA and sST2 measurements. UA was evaluated continuously and by rank-based quartiles; sST2 was evaluated continuously and in exploratory sample-median combined groups. Cardiovascular death was the primary outcome and major adverse cardiovascular events (MACE) was secondary. Cox and Fine-Gray models were used, and UA Q4 × sST2-high was the main categorical interaction analysis.
RESULTS: During follow-up, 193 all-cause deaths, 76 cardiovascular deaths, and 91 MACE occurred. Higher log10(sST2) per standard deviation was associated with cardiovascular death (HR 1.73, 95% CI 1.34-2.23) and MACE (HR 1.59, 95% CI 1.26-2.01), whereas UA alone was not associated with these outcomes after adjustment. Q1-Q3/sST2-high had higher risk than Q1-Q3/sST2-low, but categorical interactions were non-significant for cardiovascular death (P = 0.192) and MACE (P = 0.151), and Q4 estimates were imprecise.
CONCLUSIONS: Higher sST2 was consistently associated with adverse cardiovascular outcomes, whereas UA was not a stable independent prognostic marker. Exploratory subgroup differences do not establish UA-dependent effect modification and require external validation.
METHODS: This retrospective secondary analysis included 358 MHD patients with baseline UA and sST2 measurements. UA was evaluated continuously and by rank-based quartiles; sST2 was evaluated continuously and in exploratory sample-median combined groups. Cardiovascular death was the primary outcome and major adverse cardiovascular events (MACE) was secondary. Cox and Fine-Gray models were used, and UA Q4 × sST2-high was the main categorical interaction analysis.
RESULTS: During follow-up, 193 all-cause deaths, 76 cardiovascular deaths, and 91 MACE occurred. Higher log10(sST2) per standard deviation was associated with cardiovascular death (HR 1.73, 95% CI 1.34-2.23) and MACE (HR 1.59, 95% CI 1.26-2.01), whereas UA alone was not associated with these outcomes after adjustment. Q1-Q3/sST2-high had higher risk than Q1-Q3/sST2-low, but categorical interactions were non-significant for cardiovascular death (P = 0.192) and MACE (P = 0.151), and Q4 estimates were imprecise.
CONCLUSIONS: Higher sST2 was consistently associated with adverse cardiovascular outcomes, whereas UA was not a stable independent prognostic marker. Exploratory subgroup differences do not establish UA-dependent effect modification and require external validation.