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Sugar-sweetened beverage consumption and the progression of chronic kidney disease in the Multi-Ethnic Study of Atherosclerosis (MESA)^1,2,3

¹ From the Department of Medicine, Division of Nephrology, Columbia University Medical Center, New York, NY (ASB); the Department of Biostatistics, University of Washington School of Public Health, Seattle, WA (RK); the Departments of Epidemiology and Nutrition (KH), University of North Carolina, Gillings School of Global Public Health, Chapel Hill, NC; the Department of Preventive Medicine and Epidemiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (DAS); the Division of Public Health Sciences, Wake Forest University Health Sciences, Winston-Salem, NC (GLB); and the Department of Medicine, Division of Nephrology and Hypertension, University of North Carolina School of Medicine, Chapel Hill, NC (PJK).

² Supported by contracts N01-HC-95159 through N01-HC-95169 from the National Heart, Lung, and Blood Institute.

³ Address reprint requests and correspondence to AS Bomback, Columbia University, Division of Nephrology, 622 West 168th Street, PH 4-124, New York, NY 10032. E-mail: asb68{at}columbia.edu.

Background: Recent studies have examined sugar-sweetened soda consumption in relation to early markers of kidney disease, but to date there have been no investigations of whether sugar-sweetened beverage consumption affects preexistent chronic kidney disease (CKD).

Objective: This prospective cohort study of 447 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) with preexistent CKD examined the association between sugar-sweetened beverage consumption (<1 drink/wk, 1–6 drinks/wk, and 1 drink/d) and progression of CKD.

Design: β-Coefficients for continuous outcomes of changes in estimated glomerular filtration rate (eGFR) and urinary albumin to creatinine ratio (UACR) were calculated by using linear regression. Odds ratios for binary outcomes of accelerated decline in eGFR, defined as >2 mL · min^–1 · 1.73 m^–2 per year, and clinically significant progression of albuminuria (defined as attainment of UACR 30 mg/g for participants without microalbuminuria at visit 1 or a 25% increase in UACR for participants with baseline microalbuminuria) were evaluated by using logistic regression.

Results: The mean (±SD) baseline eGFR was 52 ± 6 mL · min^–1 · 1.73 m^–2 per year, and median baseline UACR was 6.3 mg/g (interquartile range: 3.5–17.6). Univariate and multivariate analyses showed no association between sugar-sweetened beverage consumption and rate of eGFR decline or changes in urinary albumin to creatinine ratio. The multivariate odds ratios comparing participants who drank 1 sugary beverage daily with those who drank 1 beverage weekly were 0.62 (95% CI: 0.27, 1.41) for accelerated eGFR decline and 1.51 (95% CI: 0.49, 4.62) for clinically significant progression of albuminuria.

Conclusion: A higher consumption of sugar-sweetened beverages was not associated with disease progression, on the basis of either eGFR or the urinary albumin to creatinine ratio, in MESA participants with preexistent CKD.