Key result
Hyperuricemia was associated with a 27% increased risk of all-cause mortality (HR 1.27) and a 36% increased risk of cardiovascular mortality (HR 1.36) in patients with cardiorenal syndrome.
Why the study?
Serum uric acid is associated with adverse outcomes in heart failure, but whether this association persists in cardiorenal syndrome remains inconclusive.
Does hyperuricemia increase the risk of mortality, MACE, and heart failure hospitalization in patients with cardiorenal syndrome?
Cohort (n=1,284)
Yes
Does hyperuricemia increase the risk of mortality, MACE, and heart failure hospitalization in patients with cardiorenal syndrome?
Hazard Ratio: 1.27 (95% CI 1.08–1.49)
p-value: p=0.004
Hyperuricemia is an independent predictor of increased all-cause and cardiovascular mortality, as well as short-term MACE and heart failure hospitalization, in patients with cardiorenal syndrome.
Hyperuricemia signals higher mortality risk in HF with CRS; extends prior observations but leaves causality and intervention effects open.
Serum uric acid (UA) has been associated with adverse outcomes in patients with heart failure. However, it remains inconclusive whether such association persists in patients with cardiorenal syndrome (CRS). In a nationwide prospective cohort from China, 4907 adults hospitalized for heart failure were enrolled. Of them, 1284 had an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m 2 at admission were included in this study. The Cox regression model was employed to evaluate the relationship between UA levels and mortality, major cardiovascular events (MACE), and hospitalization for heart failure (HHF). Additionally, Harrell’s concordance index was utilized to assess the incremental value of UA levels in predicting mortality. During a median follow-up of 3.28 years, hyperuricemia was associated with a 27 % increased risk of all-cause mortality (HR 1.27, 95 % confidence interval [CI] 1.08–1.49) and a 36 % increased risk of cardiovascular mortality (HR 1.36, 95 % CI 1.11–1.65), regardless of patients' eGFR levels. This relationship remained consistent throughout the whole follow-up period. Hyperuricemia increased the risk of 3-month MACE by 39 % (HR 1.39, 95 % CI 1.03–1.88), 3-month HHF by 47 % (HR 1.47, 95 % CI 1.11–1.95), and 1-year MACE by 26 % (HR 1.26, 95 % CI 1.02–1.57). The additive effect of uric acid levels in predicting mortality was also confirmed. Serum UA levels possess significant value in prognosis of mortality, MACE, and HHF among patients with CRS. These findings underscore the importance of monitoring serum UA in the management of patients with CRS, as UA may provide valuable insights into risk stratification. • A first study explored the effect of uric acid in patients with cardiorenal syndrome. • Hyperuricemia increased the risk of mortality in patients with cardiorenal syndrome. • The relationship between uric acid and mortality was independent of eGFR levels. • Hyperuricemia only added the short-term risk of rehospitalization for HF and MACE. • We offered a novel perspective on the clinical management of cardiorenal syndrome.
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Chen et al. (2025) conducted a cohort in Cardiorenal syndrome (n=1,284). Hyperuricemia vs. Non-hyperuricemia was evaluated on All-cause mortality (HR 1.27, 95% CI 1.08-1.49, p=0.004). Hyperuricemia was associated with a 27% increased risk of all-cause mortality (HR 1.27) and a 36% increased risk of cardiovascular mortality (HR 1.36) in patients with cardiorenal syndrome.
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