Ann A Wang1, Xuan Cai2, Anand Srivastava2,3, Pottumarthi V Prasad4, Stuart M Sprague5,6, James Carr7, Myles Wolf8,9, Joachim H Ix10, Geoffrey A Block11, Michel Chonchol12, Kalani L Raphael13, Alfred K Cheung14, Dominic S Raj15, Jennifer J Gassman16, Amir Ali Rahsepar17, John P Middleton9, Linda F Fried18, Roberto Sarnari7, Tamara Isakova2,3, Rupal Mehta2,3,19. 1. Graduate Medical Education, Feinberg School of Medicine, Northwestern University, Chicago, Illinois. 2. Center for Translational Metabolism and Health, Feinberg School of Medicine, Northwestern University, Chicago, Illinois. 3. Division of Nephrology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois. 4. Department of Radiology, NorthShore University Health System Evanston, Evanston, Illinois. 5. Division of Nephrology and Hypertension, NorthShore University Health System, Evanston, Illinois. 6. University of Chicago Pritzker School of Medicine, Chicago, Illinois. 7. Department of Radiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois. 8. Division of Nephrology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina. 9. Duke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina. 10. Division of Nephrology, Department of Medicine, University of San Diego School of Medicine and Veterans Affairs San Diego Healthcare System, San Diego, California. 11. Reata Pharmaceuticals, Irving, Texas. 12. Division of Renal Disease/Hypertension, Department of Internal Medicine, University of Colorado Hospitals, Aurora, Colorado. 13. Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University and Veterans Affairs Portland Health Care System, Portland, Oregon. 14. Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah Health, Salt Lake City, Utah. 15. Division of Kidney Diseases and Hypertension, George Washington University School of Medicine, Washington, DC. 16. Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio. 17. Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland. 18. Renal Section, Veterans Affairs Pittsburgh Healthcare System and Department of Medicine, Renal-Electrolyte Division, University of Pittsburgh, Pittsburgh, Pennsylvania. 19. Division of Nephrology, Department of Medicine, Jesse Brown Veterans Administration Medical Center, Chicago, Illinois.
Abstract
Background: Individuals with CKD have a high burden of cardiovascular disease (CVD). Abnormalities in cardiac structure and function represent subclinical CVD and can be assessed by cardiac magnetic resonance imaging (cMRI). Methods: We investigated differences in cMRI parameters in 140 individuals with CKD stages 3b-4 who participated in the CKD Optimal Management with BInders and NicotinamidE (COMBINE) trial and in 24 age- and sex-matched healthy volunteers. Among COMBINE participants, we examined the associations of eGFR, urine albumin-creatinine ratio (UACR), phosphate, fibroblast growth factor 23 (FGF23), and parathyroid hormone (PTH) with baseline (N=140) and 12-month change (N=112) in cMRI parameters. Results: Mean (SD) ages of the COMBINE participants and healthy volunteers were 64.9 (11.9) and 60.4 (7.3) years, respectively. The mean (SD) baseline eGFR values in COMBINE participants were 32.1 (8.0) and 85.9 (16.0) ml/min per 1.73 m2 in healthy volunteers. The median (interquartile range [IQR]) UACR in COMBINE participants was 154 (20.3-540.0) mg/g. Individuals with CKD had lower mitral valve E/A ratio compared with healthy volunteers (for CKD versus non-CKD, β estimate, -0.13; 95% CI, -0.24 to -0.012). Among COMBINE participants, multivariable linear regression analyses showed that higher UACR was significantly associated with lower mitral valve E/A ratio (β estimate per 1 unit increase in natural-log UACR, -0.06; 95% CI, -0.09 to -0.03). This finding was preserved among individuals without baseline CVD. UACR was not associated with 12-month change in any cMRI parameter. eGFR, phosphate, FGF23, and PTH were not associated with any cMRI parameter in cross-sectional or change analyses. Conclusions: Individuals with CKD stages 3b-4 have evidence of cMRI abnormalities. Albuminuria was independently associated with diastolic dysfunction, as assessed by mitral valve E/A ratio, in individuals with CKD with and without clinical CVD. Albuminuria was not associated with change in any cMRI parameter.
Background: Individuals with CKD have a high burden of cardiovascular disease (CVD). Abnormalities in cardiac structure and function represent subclinical CVD and can be assessed by cardiac magnetic resonance imaging (cMRI). Methods: We investigated differences in cMRI parameters in 140 individuals with CKD stages 3b-4 who participated in the CKD Optimal Management with BInders and NicotinamidE (COMBINE) trial and in 24 age- and sex-matched healthy volunteers. Among COMBINE participants, we examined the associations of eGFR, urine albumin-creatinine ratio (UACR), phosphate, fibroblast growth factor 23 (FGF23), and parathyroid hormone (PTH) with baseline (N=140) and 12-month change (N=112) in cMRI parameters. Results: Mean (SD) ages of the COMBINE participants and healthy volunteers were 64.9 (11.9) and 60.4 (7.3) years, respectively. The mean (SD) baseline eGFR values in COMBINE participants were 32.1 (8.0) and 85.9 (16.0) ml/min per 1.73 m2 in healthy volunteers. The median (interquartile range [IQR]) UACR in COMBINE participants was 154 (20.3-540.0) mg/g. Individuals with CKD had lower mitral valve E/A ratio compared with healthy volunteers (for CKD versus non-CKD, β estimate, -0.13; 95% CI, -0.24 to -0.012). Among COMBINE participants, multivariable linear regression analyses showed that higher UACR was significantly associated with lower mitral valve E/A ratio (β estimate per 1 unit increase in natural-log UACR, -0.06; 95% CI, -0.09 to -0.03). This finding was preserved among individuals without baseline CVD. UACR was not associated with 12-month change in any cMRI parameter. eGFR, phosphate, FGF23, and PTH were not associated with any cMRI parameter in cross-sectional or change analyses. Conclusions: Individuals with CKD stages 3b-4 have evidence of cMRI abnormalities. Albuminuria was independently associated with diastolic dysfunction, as assessed by mitral valve E/A ratio, in individuals with CKD with and without clinical CVD. Albuminuria was not associated with change in any cMRI parameter.
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