Georgios Vavilis1, Magnus Bäck2, Giuseppe Occhino3, Marco Trevisan4, Rino Bellocco3, Marie Evans5, Bengt Lindholm5, Karolina Szummer6, Juan Jesus Carrero4. 1. Department of Medicine, Karolinska Institute, Huddinge, Stockholm, Sweden; Theme of Heart and Vessels, Division of Coronary and Valvular Heart Disease, Karolinska University Hospital, Stockholm, Sweden; Functional Area of Emergency Medicine, Karolinska University Hospital, Huddinge, Stockholm, Sweden. Electronic address: georgios.vavilis@sll.se. 2. Theme of Heart and Vessels, Division of Coronary and Valvular Heart Disease, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine, Karolinska Institute, Solna, Stockholm, Sweden. 3. Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden; Department of Statistics and Quantitative Methods, University of Milano-Bicocca, Milan, Italy. 4. Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden. 5. Department of Clinical Science, Intervention, and Technology, Karolinska Institute, Stockholm, Sweden. 6. Department of Medicine, Karolinska Institute, Huddinge, Stockholm, Sweden; Theme of Heart and Vessels, Division of Coronary and Valvular Heart Disease, Karolinska University Hospital, Stockholm, Sweden. Electronic address: https://twitter.com/karolinskainst.
Abstract
BACKGROUND: Chronic kidney disease (CKD) and aortic stenosis (AS) share many risk factors. OBJECTIVES: This study sought to evaluate whether kidney dysfunction is associated with the development of AS in the community. METHODS: The study included 1,121,875 Stockholm citizens without a prior diagnosis of AS from the SCREAM (Stockholm CREAtinine Measurements) project. Estimated glomerular filtration rate (eGFR) (ml/min/1.73 m2) was calculated from serum creatinine. AS incidence during follow-up was ascertained by clinical diagnostic codes. The association between eGFR and AS incidence was estimated with multivariable Cox proportional hazards models. Sensitivity analyses included analysis of possible reverse causation bias by excluding the first 6 months to 2 years after enrollment and excluding individuals with comorbid heart failure. RESULTS: The median age was 50 years (interquartile range [IQR]: 36 to 64 years), and 54% of participants were women. Median eGFR was 96 ml/min/1.73 m2 (IQR: 82 to 109 ml/min/1.73 m2), and 66,949 (6.0%) participants had CKD (eGFR <60 ml/min/1.73 m2). During a median follow-up of 5.1 years (IQR: 3.3 to 6.1 years), 5,858 (0.5%) individuals developed AS (incidence rate [IR] 1.13/1,000 person-years). Compared with eGFR >90 (IR 0.34/1,000 person-years), lower eGFR strata were associated with higher hazards of AS: eGFR 60 to 90 ml/min/1.73 m2; IR: 1.88; hazard ratio (HR): 1.14; 95% confidence interval (CI): 1.05 to 1.25; eGFR 45 to 59 ml/min/1.73 m2; IR: 4.61; HR: 1.17; 95% CI: 1.05 to 1.30; eGFR 30 to 44 ml/min/1.73 m2; IR: 6.62; HR: 1.22; 95% CI: 1.07 to 1.39; and eGFR 30 ml/min/1.73 m2; IR: 8.27; HR: 1.56; 95% CI: 1.29 to 1.87. Sensitivity analysis attenuated only slightly the magnitude of the association; individuals with eGFR ≤44 ml/min/1.73 m2 remained at an approximate 20% risk of AS both when excluding events within the 2 years after baseline (HR: 1.22; 95% CI: 1.06 to 1.42) and when excluding participants with heart failure (HR: 1.20; 95% CI: 1.03 to 1.39). CONCLUSIONS: CKD, even in moderate to severe stages, is associated with an increased risk of AS.
BACKGROUND:Chronic kidney disease (CKD) and aortic stenosis (AS) share many risk factors. OBJECTIVES: This study sought to evaluate whether kidney dysfunction is associated with the development of AS in the community. METHODS: The study included 1,121,875 Stockholm citizens without a prior diagnosis of AS from the SCREAM (Stockholm CREAtinine Measurements) project. Estimated glomerular filtration rate (eGFR) (ml/min/1.73 m2) was calculated from serum creatinine. AS incidence during follow-up was ascertained by clinical diagnostic codes. The association between eGFR and AS incidence was estimated with multivariable Cox proportional hazards models. Sensitivity analyses included analysis of possible reverse causation bias by excluding the first 6 months to 2 years after enrollment and excluding individuals with comorbid heart failure. RESULTS: The median age was 50 years (interquartile range [IQR]: 36 to 64 years), and 54% of participants were women. Median eGFR was 96 ml/min/1.73 m2 (IQR: 82 to 109 ml/min/1.73 m2), and 66,949 (6.0%) participants had CKD (eGFR <60 ml/min/1.73 m2). During a median follow-up of 5.1 years (IQR: 3.3 to 6.1 years), 5,858 (0.5%) individuals developed AS (incidence rate [IR] 1.13/1,000 person-years). Compared with eGFR >90 (IR 0.34/1,000 person-years), lower eGFR strata were associated with higher hazards of AS: eGFR 60 to 90 ml/min/1.73 m2; IR: 1.88; hazard ratio (HR): 1.14; 95% confidence interval (CI): 1.05 to 1.25; eGFR 45 to 59 ml/min/1.73 m2; IR: 4.61; HR: 1.17; 95% CI: 1.05 to 1.30; eGFR 30 to 44 ml/min/1.73 m2; IR: 6.62; HR: 1.22; 95% CI: 1.07 to 1.39; and eGFR 30 ml/min/1.73 m2; IR: 8.27; HR: 1.56; 95% CI: 1.29 to 1.87. Sensitivity analysis attenuated only slightly the magnitude of the association; individuals with eGFR ≤44 ml/min/1.73 m2 remained at an approximate 20% risk of AS both when excluding events within the 2 years after baseline (HR: 1.22; 95% CI: 1.06 to 1.42) and when excluding participants with heart failure (HR: 1.20; 95% CI: 1.03 to 1.39). CONCLUSIONS: CKD, even in moderate to severe stages, is associated with an increased risk of AS.
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