Plasma lipids and risk of developing renal dysfunction: The atherosclerosis risk in communities study

Paul Muntner, Josef Coresh, J. Clinton Smith, John Eckfeldt, Michael J. Klag

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561 Scopus citations


Background: Animal and in vitro data suggest that dyslipidemia plays an important role in the initiation and progression of chronic renal disease, but few prospective studies have been conducted in humans. Methods: We studied the relationship of plasma lipids to a rise in serum creatinine of 0.4 mg/dL or greater in 12,728 Atherosclerosis Risk in Communities (ARIC) participants with baseline serum creatinine that was less than 2.0 mg/dL in men and less than 1.8 mg/dL in women. Results: During a mean follow-up of 2.9 years, 191 persons had a rise in creatinine of 0.4 mg/dL or greater, yielding an incidence rate of 5.1 per 1000 person years. Individuals with higher triglycerides and lower high-density lipoprotein (HDL) and HDL-2 cholesterol at baseline were at increased risk for a rise in creatinine after adjustment for race, gender, baseline age, diabetes, serum creatinine, systolic blood pressure, and antihypertensive medication use (all P trends ≤0.02). The adjusted relative risk for the highest versus lowest quartile of triglycerides was 1.65 (95% CI, 1.1, 2.5, P = 0.01) and for HDL was 0.47 (95% CI, 0.3, 0.8, P = 0.003). These associations were significant in participants with normal creatinine (defined as < 1.4 mg/dL for men and <1.2 mg/dL for women), with diabetes, and without diabetes. The effect of high triglycerides was independent of plasma glucose, but was weaker and less consistent after further adjustment for fasting insulin in nondiabetics. Conclusions: High triglycerides and low HDL cholesterol, but not low-density lipoprotein cholesterol, predict an increased risk of renal dysfunction. The treatment of these lipid abnormalities may decrease the incidence of early renal disease.

Original languageEnglish (US)
Pages (from-to)293-301
Number of pages9
JournalKidney international
Issue number1
StatePublished - 2000

Bibliographical note

Funding Information:
The ARIC study is carried out as a collaborative study supported by Contracts N01-HC-55015, N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, and N01-HC-55022 from the National Heart, Lung, and Blood Institute. Dr. Muntner was supported by National Institutes of Health training grant T32HL07024-23. Dr. Coresh was supported by grants from the National Institute of Diabetes Digestive and Kidney Disease (DK48362) and the National Center for Research Resources (GCRC grant RR00722). We wish to thank the staff at the ARIC field centers and the coordinating center. In particular, the following persons are acknowledged: Phyllis Johnson, Marilyn Knowles, and Melisa LaVergne from the University of North Carolina at Chapel Hill; Amy Haire, Delilah Posey, and Leslie Angel-Potter from the University of North Carolina at Winston Salem; Mary-Louise Lauffer, Suzanne Pillsbury, and Anne Safrit from Wake Forest University, Winston Salem; Cora L.K. Peoples, Cecile Snell, and Betty S. Warren from University of Mississippi Medical Center at Jackson; Molly Harrington, Darlene Heath, and Eli Justiniano from University of Minnesota, Minneapolis Center; Sunny Harrell, Patricia Hawbeaker, and Joan Nelling from The Johns Hopkins University, Baltimore; Susan Mitterling, Ashley Ewing, and R. Christy Moore from the University of Texas Medical School at Houston; Doris J. Harper, Charles E. Rhodes, and Julita Samoro from Methodist Hospital Atherosclerosis Clinical Laboratory, Houston; and Debbie Rubin Williams, Patsy Tacker, and Lily Wang from the ARIC Coordinating Center at the University of North Carolina at Chapel Hill.


  • Cholesterol
  • Chronic renal disease
  • Glomerular injury
  • Progression of renal disease
  • Triglycerides


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