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Author Notes:

C. Michael Stein, MBChB, 560 RRB, Division of Clinical Pharmacology, School of Medicine, Vanderbilt University, 23rd Ave. S at Pierce Avenue, Nashville, TN37232-6602, michael.stein@vanderbilt.edu, Tel: 615-936-3420, FAX:615-936-2746.

None of the authors has a conflict of interest related to this work.

Subjects:

Research Funding:

Supported by NIH grants HL65082, GM07569, UL1 RR024975 from NCRR/NIH; P60 AR056116; and the Dan May Chair in Medicine.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Rheumatology
  • atherosclerosis
  • cystatin C
  • inflammation
  • renal function
  • systemic lupus erythematosus
  • CHRONIC KIDNEY-DISEASE
  • CORONARY-ARTERY ATHEROSCLEROSIS
  • MILD RENAL-INSUFFICIENCY
  • CARDIOVASCULAR-DISEASE
  • ELDERLY PERSONS
  • REACTIVE PROTEIN
  • BODY-COMPOSITION
  • HEART-DISEASE
  • RISK-FACTORS
  • MORTALITY

Cystatin C is associated with inflammation but not atherosclerosis in systemic lupus erythematosus

Tools:

Journal Title:

Lupus

Volume:

Volume 21, Number 3

Publisher:

, Pages 279-287

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Background: Even mild renal impairment is associated with increased atherosclerosis and cardiovascular mortality. Cystatin C, a novel measure of renal function, is more sensitive than conventional creatinine-based measures for the detection of subtle renal impairment. Increased cystatin concentrations are also associated with cardiovascular risk, independently of conventional measures of renal function. This study examined the hypothesis that cystatin C is elevated in systemic lupus erythematosus (SLE) and is associated with coronary atherosclerosis. Methods: Serum cystatin C, creatinine, tumor necrosis factor (TNF)-α, interleukin (IL)-6, coronary artery calcium score (CACS), Framingham risk score (FRS), Modified Diet in Renal Disease estimated glomerular filtration rate (MDRD-eGFR), and other clinical parameters were measured in 118 patients with SLE and 83 control subjects. The independent association between concentrations of cystatin C and SLE was evaluated using multivariable linear regression models, and the relationship between renal measures and coronary calcium was assessed with multivariable proportional odds logistic regression models. Results: Cystatin C, but not other measures of renal function, was significantly higher in patients with SLE than in controls (1.09 [interquartile range, IQR: 0.85-1.28] mg/l vs. 0.89 [IQR: 0.76-0.99] mg/l; p < 0.001 after adjustment for age, race, sex and MDRD-eGFR). Cystatin C was significantly associated with SLICC (p = 0.04), erythrocyte sedimentation rate (ESR) (p = 0.02), TNF-α (p = 0.008) and IL-6 (p = 0.01) after adjustment for age, race, and sex. Cystatin C was not significantly correlated with coronary calcium score in SLE (rho=0.096, p = 0.31) and the association remained non-significant after adjustment for age, race, sex, and Framingham risk score (p = 0.99). Conclusions: Cystatin C was higher in patients with SLE than in control subjects even after adjustment for conventional measures of renal function. Cystatin C was significantly correlated with several markers of inflammation in SLE but was not associated with coronary atherosclerosis. Subtle renal dysfunction does not appear to be directly associated with accelerated atherosclerosis in SLE.

Copyright information:

© The Author(s), 2012.

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