Key result
In adults without prior CVD, eGFRcysC <60 mL/min/1.73 m2 was associated with 56% and 73% increased risks for all-cause and CVD mortality compared to >90 mL/min/1.73 m2.
Why the study?
Does reduced cystatin C-based eGFR predict all-cause and cardiovascular disease mortality in adults without a history of CVD?
Cohort (n=9,353)
Does reduced cystatin C-based eGFR predict all-cause and cardiovascular disease mortality in adults without a history of CVD?
Effect estimate: 56% increase in risk
Reduced cystatin C-based eGFR is associated with increased all-cause and CVD mortality, and adding CKD measures improves risk stratification primarily among low-risk individuals.
May enhance mortality risk stratification in low-risk adults without CVD; extends observational CKD data but leaves open prospective validation.
Aims Uncertainties about the role of cystatin C‐based estimated glomerular filtration rate (eGFR) in the prediction of cardiovascular disease (CVD) beyond traditional CVD risk factors remain. We assessed contributions of eGFR to CVD and mortality in the general population. Methods Using 14 year follow‐up data on 9353 adults without a reported history of CVD from the Australian Diabetes, Obesity and Lifestyle study, we assessed the contributions of eGFR (assessed by cystatin C (eGFRcysC) and serum creatinine (eGFRcr) and albuminuria (uACR) to total and CVD mortality. Results After adjusting for age, sex, CVD risk factors and uACR, compared with an eGFRcysC>90 mL/min per 1.73 m2, eGFRcysC<60 mL/min per 1.73 m2was associated with 56% and 73% increases in the risks for all‐cause and CVD mortality, respectively. The respective changes for the c‐statistic when eGFRcysCwas added to a risk prediction model were 0.003 (95% confidence interval: 0.001 to 0.005) and 0.002 (95% confidence interval: −0.001 to 0.006). The net proportion of non‐events assigned a lower‐risk category significantly improved with the addition of eGFR (non‐event net reclassification index eGFRcr: 1.0% and eGFRcysC: 1.5%) for all‐cause mortality, but for CVD mortality, improvements were only significant when eGFR was combined with uACR. The net proportion of events assigned a higher‐risk category was not significantly improved. Conclusion In our community‐based cohort, reduced eGFRcysCwas associated with all‐cause and CVD mortality. The addition of chronic kidney disease measures to risk prediction models improved overall risk stratification among those at low risk as opposed to those at high baseline risk of mortality.
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Barr et al. (2016) conducted a cohort in General population without cardiovascular disease (n=9,353). Reduced eGFRcysC (<60 mL/min per 1.73 m2) vs. eGFRcysC >90 mL/min per 1.73 m2 was evaluated on All-cause mortality (56% increase in risk). In adults without prior CVD, eGFRcysC <60 mL/min/1.73 m2 was associated with 56% and 73% increased risks for all-cause and CVD mortality compared to >90 mL/min/1.73 m2.
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