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Updated: Jul 3, 2026

A Semi-Automated and Reproducible Biological-Based Method to Quantify Calcium Deposition In Vitro
Published on: June 2, 2022
Indexes of kidney function and coronary artery and abdominal aortic calcium (from the Framingham Offspring Study)
Nisha I Parikh1, Shih-Jen Hwang, Martin G Larson
1National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, Massachusetts, USA.
Insights
Chronic kidney disease (CKD) and kidney function markers like cystatin C and microalbuminuria are not linked to subclinical atherosclerosis (coronary artery calcium or abdominal aortic calcium) after accounting for cardiovascular risk factors.
Area of Science:
- Nephrology
- Cardiology
- Radiology
Background:
- Subclinical atherosclerosis, indicated by coronary artery calcium (CAC) and abdominal aortic calcium (AAC), is a key predictor of cardiovascular events.
- The relationship between moderate chronic kidney disease (CKD) and kidney function markers with subclinical atherosclerosis remains unclear.
Purpose of the Study:
- To investigate the association between CKD, cystatin C (cysC), and microalbuminuria (MA) with CAC and AAC.
- To determine if kidney function measures predict subclinical atherosclerosis in a well-characterized cohort.
Main Methods:
- Logistic and linear regression analyses were performed on Framingham Heart Study Offspring participants (n=1,179).
- CKD (glomerular filtration rate <60 ml/min/1.73 m(2)), cysC, and MA were assessed in relation to CAC and AAC measured by multidetector computed tomography.
- Analyses were adjusted for major cardiovascular disease risk factors.
Main Results:
- CKD was not significantly associated with CAC (OR 1.18) or AAC (OR 1.11) in multivariable models.
- Microalbuminuria (MA) showed no association with CAC (OR 0.81) or AAC.
- Cystatin C (cysC) was associated with CAC in age- and gender-adjusted models but not after multivariable adjustment.
Conclusions:
- Moderate CKD, cysC, and MA are not independently associated with CAC or AAC in this cohort.
- These findings suggest that traditional cardiovascular risk factor adjustments sufficiently explain the link between kidney function and subclinical atherosclerosis.
Abstract:
It is uncertain whether moderate chronic kidney disease (CKD) or measures of kidney function are associated with subclinical atherosclerosis as represented by coronary artery calcium (CAC) or abdominal aortic calcium (AAC). We used logistic and linear regression analyses to relate CKD (glomerular filtration rate <60 ml/min/1.73 m(2)), cystatin C (cysC), and microalbuminuria (MA) with CAC and AAC obtained using multidetector computed tomography in Framingham Heart Study Offspring participants (mean age 59 years, 55.3% women). Increased CAC and AAC were defined as > or =90th percentile age- and gender-specific cutpoints based on a healthy referent sample. Major cardiovascular disease risk factors were accounted for in multivariable models. Of 1,179 participants, 1,174 had AAC measurements and 1,147 had CAC measurements, 6.3% had CKD, and 8.3% had MA. CKD was not associated with CAC (multivariable-adjusted odds ratio [OR] for CKD 1.18, 95% confidence interval 0.59 to 2.36, p = 0.63) or AAC (multivariable-adjusted OR for CKD 1.11, 95% confidence interval 0.61 to 2.04, p = 0.73). CysC was associated with CAC in age- and gender-adjusted but not in multivariable models (age- and gender-adjusted OR for log cysC per SD increment and CAC 1.19, 95% confidence interval 1.01 to 1.41, p = 0.04; multivariable-adjusted OR 1.14, 95% confidence interval 0.95 to 1.38, p = 0.15). MA was not associated with CAC (OR 0.81, 95% confidence interval 0.41 to 1.61, p = 0.54). Neither cysC nor MA was significantly associated with AAC in age- and gender- or multivariable-adjusted models. In conclusion, CKD, cysC, and MA are not associated with CAC or AAC when accounting for cardiovascular disease risk factors.
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