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Published ahead of print on June 18, 2008
Clin J Am Soc Nephrol 3: 1289-1295, 2008
© 2008 American Society of Nephrology
doi: 10.2215/CJN.00010108

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Clinical Nephrology

Coronary Artery Calcification, ADMA, and Insulin Resistance in CKD Patients

Shuzo Kobayashi, Machiko Oka, Kyoko Maesato, Ryota Ikee, Tsutomu Mano, Moriya Hidekazu, and Takayasu Ohtake

Department of Nephrology, and Kidney & Dialysis Center, Shonan Kamakura General Hospital, Kamakura, Kanagawa, Japan

Correspondence: Dr. Shuzo Kobayashi, Shonan Kamakura General Hospital, 1202–1 Yamazaki, Kamakura, Kanagawa, 247-8533, Japan. Phone: 81-467-32-9071; Fax: 81-467-32-9148; E-mail: shuzo{at}shonankamakura.or.jp

Background and objectives: It is known that coronary artery calcification (CAC) develops in chronic kidney disease (CKD) before initiation of renal replacement therapy, and factors associated with CKD mineral and bone disorders (CKD-MBDs) are involved. However, little information is available about any association between plasma levels of asymmetric dimethylarginine (ADMA), insulin resistance, and CAC.

Design, setting, participants, & measurements: A total of 111 CKD patients (79 men, 32 women; glomerular filtration rate [GFR] median, 33.7 ml/min per 1.73 m2), free of cardiovascular disease, were consecutively recruited along with 30 age-matched healthy subjects. Coronary artery calcification scores (CACS) were measured by multidetector-row CT according to Agatston score.

Results: In CKD patients, CACS was distributed widely from 0 to 2901, while in age-matched, healthy control subjects (n = 30), CACS showed a range from 0 to 307. GFR had a significant negative correlation with CACS. Plasma ADMA levels were negatively correlated with GFR and positively correlated with CACS. When CACS was divided into quartiles (<50, n = 56; 50 to 300, n = 24; 300 to 600, n = 14; >600, n = 17), the patients with CACS >600 had significantly higher values of HOMA-IR, plasma ADMA levels, and fibrinogen along with serum levels of phosphorus, compared with those in patients having CACS <50. Multivariate regression analysis determined HOMA-IR as an independent contributing factor to CACS.

Conclusions: CAC becomes more prevalent and severe with a decline in GFR, and plasma ADMA levels and insulin resistance, independent of factors associated with CKD-MBD, are correlated with CAC.







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