Key result
Heart failure is linked to more than double the annual eGFR decline versus matched controls.
Why the study?
Does heart failure accelerate the longitudinal decline in eGFR compared to matched community comparators?
Cohort (n=2,007)
Does heart failure accelerate the longitudinal decline in eGFR compared to matched community comparators?
Absolute Event Rate: -4.23% vs -1.9%
p-value: p=<0.001
Heart failure is associated with a significantly faster longitudinal decline in kidney function compared to community comparators, particularly in those with metabolic comorbidities.
Introduction: Chronic kidney disease affects nearly half of heart failure (HF) patients, underscoring the importance of regular kidney function monitoring. However, longitudinal trajectories of kidney function in HF are not well characterized. Identifying clinical factors linked to long-term changes is critical for improving monitoring and informing early clinical decisions. Hypothesis: We hypothesized that longitudinal kidney function and its associations with clinical variables in HF patients differ from that of demographically similar comparators from the same community. Methods: We analyzed patients with validated HF from a community-based cohort and comparators individually matched to age and sex selected from participants in the Mayo Clinic Biobank cohort. Individuals with end-stage kidney disease, dialysis or kidney transplantation prior to enrollment were excluded. Serum creatinine-based estimated glomerular filtration rate (eGFR) from outpatient and inpatient visits was assessed from enrollment for up to 10 years of follow-up. The median of eGFR for 90-day intervals was used to estimate the follow-up eGFR (Figure 1) . We modeled percentage change from baseline and fit linear mixed-effect models with time, HF status, and their interaction to test whether the eGFR trajectories differed between the two groups. In addition, we examined the association between eGFR trajectories and clinical variables. Results: We studied 1182 HF patients and 825 comparators with at least three eGFR measurements. Median follow-up was 5 years (IQR: 3-10) for HF patients and 8 years (6-9) for comparators. In total, 16245 serum creatinine measurements from HF patients and 9858 from comparators were analyzed. Median age at enrollment was 76 years (67-84) for HF patients and 78 years (70-83) for comparators. A greater decline in percentage change in eGFR was observed in HF patients (-4.23%, 95% CI: -4.75 to -3.70% per year) than in comparators (-1.90%, 95% CI: -2.51 to -1.29% per year; P<0.001, Figure 2 ). Among HF patients, the decline in percentage change in eGFR was greater in the presence of diabetes, hyperlipidemia, or a higher comorbidity burden. Conclusions: In this community study, HF patients exhibited a greater percentage decline in eGFR compared to community comparators. Among HF patients, eGFR decline was more strongly associated with comorbidities—particularly metabolic risk factors—highlighting the relevance of the cardiovascular-kidney-metabolic syndrome in HF.
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Kim et al. (2026) conducted a cohort in Heart failure (n=2,007). Heart failure vs. Matched community comparators without heart failure was evaluated on Annual percentage change in estimated glomerular filtration rate (eGFR) (p=<0.001). Heart failure patients exhibited a significantly greater annual percentage decline in estimated glomerular filtration rate compared to matched community comparators (-4.23% vs -1.90%; P<0.001).
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