Lipoprotein abnormalities associated with mild impairment of kidney function in the multi-ethnic study of atherosclerosis.
OBJECTIVE
Impaired kidney function is associated with increased risk for cardiovascular disease and may progress over time to end-stage renal disease. Abnormal lipoprotein metabolism has been implicated as a possible cause of these complications, but lipoproteins have not been described at the earliest stages of kidney disease.


METHODS
This study examined cross-sectional associations of serum cystatin C with conventional lipid measurements and detailed nuclear magnetic resonance lipoprotein measurements in the community-based Multi-Ethnic Study of Atherosclerosis. A total of 5109 participants with estimated glomerular filtration rate > or =60 ml/min per 1.73 m(2) were included in analyses.


RESULTS
Adjusting for age, gender, race/ethnicity, diabetes, impaired fasting glucose, BP, smoking, medications, body mass index, and albuminuria, greater cystatin C concentrations were associated with progressively unfavorable lipid and lipoprotein concentrations, including greater triglyceride concentration (+22 mg/dl, comparing fifth versus first quintiles of cystatin C) and lesser high-density lipoprotein cholesterol concentration (-7 mg/dl) but not with low-density lipoprotein cholesterol measured using conventional methods. When low-density lipoprotein particle subclasses were examined in more detail using nuclear magnetic resonance, greater cystatin C was associated with greater concentrations of atherogenic small low-density lipoprotein particles (+63 nmol/L) and intermediate-density lipoprotein particles (+6 nmol/L) and with a decrease in mean low-density lipoprotein particle size.


CONCLUSIONS
Lipoprotein abnormalities are present with milder degrees of renal impairment than previously recognized, and abnormalities in low-density lipoprotein particle distribution may not be appreciated using conventional lipid measurements. These abnormalities may contribute to kidney disease progression and/or cardiovascular disease.
Division of Nephrology, University of Washington, Seattle, Washington 98195, USA. deboer@u.washington.edu
Ian H
IH
de Boer
Brad C
BC
Astor
Holly
H
Kramer
Walter
W
Palmas
Stephen L
SL
Seliger
Michael G
MG
Shlipak
David S
DS
Siscovick
Michael Y
MY
Tsai
Bryan
B
Kestenbaum
D000368:Aged; D000369:Aged, 80 and over; D044466:Asian People / Q000706:statistics & numerical data; D050197:Atherosclerosis / Q000208:ethnology*; D044383:Black People / Q000706:statistics & numerical data; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003430:Cross-Sectional Studies; D055316:Cystatin C; D015891:Cystatins / Q000097:blood; D018450:Disease Progression; D005260:Female; D006630:Hispanic or Latino / Q000706:statistics & numerical data; D006801:Humans; D006949:Hyperlipidemias / Q000208:ethnology*; D007674:Kidney Diseases / Q000208:ethnology*; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011446:Prospective Studies; D012307:Risk Factors; D012720:Severity of Illness Index; D014280:Triglycerides / Q000097:blood; D044465:White People / Q000706:statistics & numerical data
C525030:CST3 protein, human; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D055316:Cystatin C; D015891:Cystatins; D008074:Lipoproteins; D014280:Triglycerides; C030104:lipoprotein cholesterol; D002784:Cholesterol