Joshua D Bundy1, Jing Chen1, Wei Yang2, Matthew Budoff3, Alan S Go4, Juan E Grunwald5, Radhakrishna R Kallem5, Wendy S Post6, Muredach P Reilly7, Ana C Ricardo8, Sylvia E Rosas9, Xiaoming Zhang2, Jiang He10. 1. Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, USA. 2. Department of Biostatistics and Epidemiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA. 3. Los Angeles Biomedical Research Institute, Los Angeles County Harbor-UCLA Medical Center, Torrance, CA, USA. 4. Division of Research, Kaiser Permanente Division of Research, Oakland, CA, USA. 5. Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA. 6. Welch Center for Prevention, Epidemiology, and Clinical Research, The Johns Hopkins University, Baltimore, MD, USA. 7. Department of Medicine, Columbia University Medical Center, New York, NY, USA. 8. Department of Medicine, University of Illinois, Chicago, IL, USA. 9. Joslin Diabetes Center, Harvard University, Boston, MA, USA. 10. Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, USA. Electronic address: jhe@tulane.edu.
Abstract
BACKGROUND AND AIMS: Coronary artery calcification (CAC) is common among patients with chronic kidney disease (CKD) and predicts the risk for cardiovascular disease (CVD). We examined the associations of novel risk factors with CAC progression among patients with CKD. METHODS: Among 1123 CKD patients in the Chronic Renal Insufficiency Cohort (CRIC) Study, CAC was measured in Agatston units at baseline and a follow-up visit using electron beam computed tomography or multidetector computed tomography. RESULTS: Over an average 3.3-year follow-up, 109 (25.1%) participants without CAC at baseline had incident CAC and 124 (18.0%) participants with CAC at baseline had CAC progression, defined as an annual increase of ≥100 Agatston units. After adjustment for established atherosclerotic risk factors, several novel risk factors were associated with changes in CAC over follow-up. Changes in square root transformed CAC score associated with 1 SD greater level of risk factors were -0.20 (95% confidence interval, -0.31 to -0.10; p < 0.001) for estimated glomerular filtration rate, 0.14 (0.02-0.25; p = 0.02) for 24-h urine albumin, 0.25 (0.15-0.34; p < 0.001) for cystatin C, -0.17 (-0.27 to -0.07; p < 0.001) for serum calcium, 0.14 (0.03-0.24; p = 0.009) for serum phosphate, 0.24 (0.14-0.33; p < 0.001) for fibroblast growth factor-23, 0.13 (0.04-0.23; p = 0.007) for total parathyroid hormone, 0.17 (0.07-0.27; p < 0.001) for interleukin-6, and 0.12 (0.02-0.22; p = 0.02) for tumor necrosis factor-α. CONCLUSIONS: Reduced kidney function, calcium and phosphate metabolism disorders, and inflammation, independent of established CVD risk factors, may progress CAC among CKD patients.
BACKGROUND AND AIMS: Coronary artery calcification (CAC) is common among patients with chronic kidney disease (CKD) and predicts the risk for cardiovascular disease (CVD). We examined the associations of novel risk factors with CAC progression among patients with CKD. METHODS: Among 1123 CKDpatients in the Chronic Renal Insufficiency Cohort (CRIC) Study, CAC was measured in Agatston units at baseline and a follow-up visit using electron beam computed tomography or multidetector computed tomography. RESULTS: Over an average 3.3-year follow-up, 109 (25.1%) participants without CAC at baseline had incident CAC and 124 (18.0%) participants with CAC at baseline had CAC progression, defined as an annual increase of ≥100 Agatston units. After adjustment for established atherosclerotic risk factors, several novel risk factors were associated with changes in CAC over follow-up. Changes in square root transformed CAC score associated with 1 SD greater level of risk factors were -0.20 (95% confidence interval, -0.31 to -0.10; p < 0.001) for estimated glomerular filtration rate, 0.14 (0.02-0.25; p = 0.02) for 24-h urine albumin, 0.25 (0.15-0.34; p < 0.001) for cystatin C, -0.17 (-0.27 to -0.07; p < 0.001) for serum calcium, 0.14 (0.03-0.24; p = 0.009) for serum phosphate, 0.24 (0.14-0.33; p < 0.001) for fibroblast growth factor-23, 0.13 (0.04-0.23; p = 0.007) for total parathyroid hormone, 0.17 (0.07-0.27; p < 0.001) for interleukin-6, and 0.12 (0.02-0.22; p = 0.02) for tumor necrosis factor-α. CONCLUSIONS: Reduced kidney function, calcium and phosphatemetabolism disorders, and inflammation, independent of established CVD risk factors, may progress CAC among CKDpatients.
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