Chronic Kidney Disease, Plasma Lipoproteins, and Coronary Artery Calcium Incidence

Objective— To determine the association of chronic kidney disease and coronary artery calcium (CAC) incidence, and the distribution of lipoproteins across categories of kidney function and their association with CAC risk. Methods and Results— We analyzed data from 2795 participants in the Multi-Ethnic Study of Atherosclerosis with no CAC (calcium score=0) at baseline enrolled at the first Multi-Ethnic Study of Atherosclerosis visit between the years 2000 and 2002. During a median follow-up of 2.4 years, incident calcium (calcium score>0 at follow-up) developed in 12%, 19%, and 27% of participants with a cystatin-c estimated glomerular filtration rate (mL/min per 1.73 m) 2 of ≥90, 60 to 89, and 30 to 59 ( P for difference <0.001), respectively. Compared with those with normal kidney function (estimated glomerular filtration rate≥90), adjusted CAC incidence risk ratios, and 95% confidence intervals (CIs) were as follows: 1.26 (95% CI, 1.04–1.52), and 1.56 (95% CI, 1.11–2.20; P trend =0.014) in those with estimated glomerular filtration rate of 60 to 89 and 30 to 59, respectively. These associations were attenuated after adjusting for a characteristic and strongly interrelated lipid phenotype (principal component 1), which was more common in those with chronic kidney disease and characterized by a predominance of triglyceride-rich lipoproteins: CAC incidence risk ratios=1.21 (95% CI, 1.00–1.46) and 1.44 (95% CI, 1.02–2.04; P trend =0.06) in those with estimated glomerular filtration rate 60 to 89 and 30 to 59, respectively, after adjusting for principal component 1. Conclusion— Chronic kidney disease is strongly associated with CAC incidence. Part of this association is mediated through a characteristic lipid phenotype comprising elevations in triglyceride-rich lipoproteins.