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Coronary calcification in chronic kidney disease: morphology, mechanisms and mortality.

Chronic kidney disease (CKD) is associated with increased cardiovascular disease (CVD) morbidity and mortality (1,2). The precise contribution of coronary atherosclerotic disease (CAD) to mortality is unclear. Although acute myocardial infarction (MI) ranks behind sudden cardiac death as a cause of fatal events, sudden cardiac death has heterogeneous causes and CAD is likely a substantial contributor (3). The burden of CAD in patients with CKD makes it imperative to identify both subclinical disease and modifiable risk factors that might be potential targets for intervention.

In patients without CKD, coronary artery calcification (CAC) has emerged as a marker of subclinical atherosclerosis. In addition to an association with traditional CAD risk factors (4,5), CAC scores are correlated with the burden of coronary atherosclerosis at coronary angiography (6,7) and histopathologically at autopsy (8). CAC has been shown to be a strong predictor of future cardiovascular events across a spectrum of CVD risk (9–11).

CAC is frequently seen in patients with all stages of CKD (12–14). As with patients with normal renal function, CAC is associated with traditional CAD risk factors (15), correlates with coronary angiography (16), and provides prognostic value (17). Morphologically, CAC histopathologic lesions in patients with CKD seem to differ from those with normal renal function. In the non-CKD setting, CAC deposition is limited almost entirely to the vessel intima in association with atherosclerosis (18). In CKD, calcification is thought to be both intimal and medial (19). Both intimal and medial CAC are likely to predict CVD …