Key result
Higher cystatin C- vs creatinine-based eGFR links to ~12% lower mortality per 10 mL/min/1.73 m² in ACS.
Why the study?
Discordance between creatinine- and cystatin C-based eGFR is associated with adverse outcomes in population-based cohorts, but its relevance in patients with ACS remained uncertain.
Does discordance between creatinine- and cystatin C-based eGFR identify long-term risks of all-cause mortality, MACE, and kidney function decline in patients hospitalized with acute coronary syndrome?
Cohort (n=808)
No
Does discordance between creatinine- and cystatin C-based eGFR identify long-term risks of all-cause mortality, MACE, and kidney function decline in patients hospitalized with acute coronary syndrome?
In patients hospitalized with ACS, having a lower cystatin C-based eGFR relative to creatinine-based eGFR identifies patients at elevated risk for long-term mortality, MACE, and renal decline, even when creatinine-based kidney function appears preserved.
Answers are grounded in this paper and cite their sources.
May aid risk stratification in ACS; extends general-population discordance findings to this high-risk setting.
BACKGROUND: Discordance between creatinine- and cystatin C-based estimated glomerular filtration rate (eGFR) is common and has been associated with adverse outcomes in population-based cohorts. However, its relevance in patients with acute coronary syndrome (ACS) remains uncertain. METHODS: We conducted a retrospective cohort study including 808 patients with ACS admitted to the Cardiac Intensive Care Unit of Marqués de Valdecilla University Hospital (Santander, Spain) between 1 January, 2012 and 31 December, 2015, for whom measurements of creatinine and cystatin C at admission were available. Discordance between creatinine- and cystatin C-based eGFR was assessed using continuous indices (eGFR difference and ratio) and categorical definitions based on a threshold of 15 mL/min/1.73m². Associations with all-cause mortality, major adverse cardiovascular events (MACE), and kidney function decline were evaluated using Cox regression models adjusted for cardiovascular risk factors and creatinine-cystatin C eGFR. RESULTS: Creatinine-cystatin C eGFR discordance was present in 44.2% of patients. Over a median follow-up of 8.4 years, lower cystatin C-based relative to creatinine-based eGFR was associated with higher risks of all-cause mortality, MACE, and kidney function decline. These associations persisted among patients with preserved creatinine-based kidney function. In adjusted models, each 10 mL/min/1.73 m² increase in eGFR difference, indicating higher eGFRcys relative to eGFRcr, was associated with lower risks of mortality (Hazard Ratio [HR] 0.88, 95% Confidence Interval [CI] 0.80-0.96) and kidney function decline (HR 0.80, 95% CI 0.71-0.91), with a similar trend for MACE (HR 0.91, 95% CI 0.83-1.00). CONCLUSIONS: In patients hospitalised with ACS, eGFR discordance reflecting lower cystatin C-based eGFR than creatinine-based eGFR is associated with adverse long-term cardiorenal outcomes, even among patients with preserved creatinine-based kidney function.
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García-Majado et al. (2026) conducted a cohort in Acute coronary syndrome (ACS) (n=808). Creatinine-cystatin C eGFR discordance (per 10 mL/min/1.73 m² increase in eGFR difference, indicating higher eGFRcys relative to eGFRcr) vs. Concordant eGFR or lower eGFRcys relative to eGFRcr was evaluated on All-cause mortality (HR 0.88, 95% CI 0.80-0.96). Each 10 mL/min/1.73 m² higher cystatin C- vs creatinine-based eGFR in ACS patients was associated with lower all-cause mortality and kidney function decline.
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