Abstract 2152: Close Bidirectional Relationship Between Chronic Kidney Disease and Atrial Fibrillation: The Niigata Preventive Medicine Study
Atrial fibrillation (AF) and chronic kidney disease share risk factors including obesity, hypertension, diabetes, and the metabolic syndrome as well as pathophysiologic mechanisms including persistent inflammation and oxidative stress. We tested the hypothesis here that two conditions are risk factors for each other. This is a prospective community-based observational cohort study based upon an annual health check-up in Niigata prefecture, Japan. We studied the association of kidney dysfunction with new-onset AF and the association of AF with development of kidney disease in 235,818 subjects (mean age, 60.9 ± 11.7 years). Development of kidney dysfunction was defined by an elevation of serum creatinine level (≥1.4 mg/dL for men, ≥1.2 mg/dL for women) or an GFR reduction (<60 ml/min/1.73 m2) in subjects without baseline kidney dysfunction. Kidney disease as risk of AF During a follow-up of 5.9 ± 2.4 years, AF developed in 2,947 subjects (1.3%). Baseline serum creatinine and GFR were associated with risk of subsequent AF (adjusted hazard ratios, HRs [95% confidence interval, CI], 1.09 [1.02–1.17] for serum creatinine [1 mg/dL increment] and 1.02 [1.00 –1.03] for GFR [10 ml/min/1.73 m2 decline]). The HRs for AF increased inversely with GFR: 1.32 (95% CI, 1.08 –1.62) for GFR 30 –59 ml/min/1.73 m2 and 1.57 (95% CI, 0.89 –2.77) for GFR <30 ml/min/1.73 m2. The effect of chronic kidney disease on risk of new-onset AF was significant after eliminating subjects with treated hypertension or diabetes. AF as risk of kidney disease During a 5.9 year follow-up, 7,791 subjects (4.0%) developed kidney dysfunction and 11,307 subjects (5.8%) developed proteinuria. Baseline AF was associated with development of kidney dysfunction (HRs [95% CI], 1.84 [1.30 –2.61] for serum creatinine-based model and 1.77 [1.50 –2.10] for GFR-based model) and proteinuria (HR [95% CI], 2.20 [1.92–2.52]). The association remained significant in subjects without treated hypertension and diabetes. Kidney dysfunction increased the risk of new-onset of AF and AF increased risk of development of kidney disease. This finding supports the concept that the two conditions share common abnormal molecular signaling pathways contributing to their pathogenesis.