Cystatin C and carotid intima-media thickness in asymptomatic adults: the Multi-Ethnic Study of Atherosclerosis (MESA).
BACKGROUND
Persons with early kidney disease have an increased risk of cardiovascular events and mortality, but the importance of accelerated atherosclerosis in promoting these outcomes is unclear. We therefore explored whether serum cystatin C level is associated with carotid intima-media thickness (IMT) in ambulatory adults without clinical heart disease.


METHODS
Cross-sectional study.


METHODS
We evaluated 6,557 ethnically diverse persons free of clinical cardiovascular disease aged 45 to 84 years at the baseline visit of the Multi-Ethnic Study of Atherosclerosis.


METHODS
Kidney function was estimated by using 2 methods: serum cystatin C level and estimated glomerular filtration rate, based on creatinine and cystatin C levels.


METHODS
Study outcomes were internal and common carotid IMT, measured by using high-resolution B-mode ultrasound. Multivariate linear and logistic regressions were used to evaluate the independent association of kidney function with carotid IMT.


RESULTS
In unadjusted linear analysis, each SD (0.23 mg/L) greater cystatin C level was associated with 0.091-mm greater internal carotid IMT (P < 0.001), but this association was diminished by 70% after adjustment for age, sex, and race/ethnicity (0.027 mm; P < 0.001) and was no longer significant after adjustment for cardiovascular risk factors (0.005 mm; P = 0.5). Similarly, the strong unadjusted associations of cystatin C level with common carotid IMT disappeared after adjustment. Chronic kidney disease, defined by using either creatinine level or cystatin C-based estimated glomerular filtration rate less than 60 mL/min/1.73 m(2), had no independent association with internal and common carotid IMT.


CONCLUSIONS
There were few participants with severe kidney disease.


CONCLUSIONS
Cystatin C level had no independent association with carotid IMT in a population free of clinical heart disease. This observation suggests that accelerated atherosclerosis is unlikely to be the primary mechanism explaining the independent association of cystatin C level with cardiovascular risk.
Bui
Anh L
AL
Department of Medicine, University of California, San Francisco, CA, USA.
Katz
Ronit
R
Kestenbaum
Bryan
B
de Boer
Ian H
IH
Fried
Linda F
LF
Polak
Joseph F
JF
Wasserman
Bruce A
BA
Sarnak
Mark J
MJ
Siscovick
David
D
Shlipak
Michael G
MG
D001741:Black or African American; D000368:Aged; D000369:Aged, 80 and over; D001213:Asian; D002339:Carotid Arteries / Q000473:pathology*; D003430:Cross-Sectional Studies; D055316:Cystatin C / Q000097:blood*; D005260:Female; D006630:Hispanic or Latino; D006801:Humans; D007674:Kidney Diseases / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D017539:Tunica Intima / Q000473:pathology*; D017540:Tunica Media / Q000473:pathology*; D044465:White People
D055316:Cystatin C