Received April 19, 2008
Accepted on October 30, 2008

ORIGINAL ARTICLES

Atheroma Progression in Chronic Kidney Disease

Claudio Rigatto ^*1, Adeera Levin , Andrew A. House , Brendan Barrett , Euan Carlisle ^||, and Adrian Fine ^*

*Department of Internal Medicine and Section of Nephrology, University of Manitoba, Winnipeg, Canada; Department of Medicine and Division of Nephrology, University of British Columbia, Vancouver Canada; Department of Medicine and Division of Nephrology, University of Western Ontario, London, Canada; Department of Medicine and Division of Nephrology, Memorial University of Newfoundland, St. John’s, Canada; and ||Department of Medicine, McMaster University, Hamilton, Canada

¹ To whom correspondence should be addressed. E-mail: crigatto{at}sbgh.mb.ca.

	Abstract

Background and objectives: Cardiovascular events are 10 to 100 times more frequent in chronic kidney disease (CKD). We tested the hypothesis that the rate of atherosclerotic plaque growth is faster in severe versus moderate CKD.

Design, setting, participants, & measurements: We performed a prospective cohort study in 318 prevalent CKD patients with initial creatinine clearance (CCr) between 20 and 50 ml/min/1.73 m². Baseline clinical and laboratory data were obtained on all patients. Plaque area was determined every 6 mo using bilateral carotid ultrasonography. Plaque area distribution was normalized using a cube root transformation. Unadjusted and adjusted associations between CCr quintiles and rate of change in the transformed plaque area were assessed using multiple linear regression.

Results: The rate of plaque progression appeared lower in patients with the lowest CCr. Median rate of plaque growth was 0.4 mm²/yr in the lowest quintile of CCr (< 23 ml/min/1.73 m²) versus 5.0 mm²/yr in the highest quintile (> 43 ml/min/1.73 m²). This association remained significant after adjustment for potential confounders. A secondary analysis using quintiles of Modification of Diet in Renal Disease (MDRD) GFR confirmed the absence of increased plaque growth at low GFR, although a reduced rate of growth in the lowest quintile of MDRD GFR was not observed.

Conclusion: We did not observe accelerated plaque growth at low levels of renal function. We suggest that mechanisms other than plaque growth are responsible for the observed excess of cardiovascular disease in CKD patients.