Published online Apr 26, 2014. doi: 10.4330/wjc.v6.i4.115
Revised: February 10, 2014
Accepted: March 13, 2014
Published online: April 26, 2014
Processing time: 127 Days and 3.7 Hours
Arterial calcification is a well-recognized complication of advanced atherosclerosis. Chronic kidney disease (CKD) is characterized by significantly more pronounced, disseminated and fast-progressing calcification of the vascular system, including the coronary arteries. New computed tomography-based imaging techniques allow for the noninvasive assessment and monitoring of calcification in different vascular sites. Coronary artery calcification (CAC) develops early in the course of CKD and is tightly associated with mineral and bone disorders, which include but are not limited to secondary hyperparathyroidism. In this review, recent data on the pathogenesis of CAC development and progression are discussed, with a special emphasis on fibroblast growth factor 23 and its co-receptor, klotho. The prevalence, progression and prognostic significance of CAC are reviewed separately for patients with end-stage renal disease treated with dialysis, kidney transplant recipients and patients with earlier stages of CKD. In the last section, therapeutic considerations are discussed, with special attention paid to the importance of treatment that addresses mineral and bone disorders of CKD.
Core tip: Vascular calcification, a common feature of advanced atherosclerosis in the general population, is extremely advanced in patients with chronic kidney disease (CKD). CKD is associated with very fast progression of vascular (and in particular coronary) calcification. Pathogenetic aspects, clinical consequences and prognostic significance of coronary artery calcification in different CKD populations are discussed in this review. Therapeutic strategies used to limit the extent of vascular calcification and to improve the prognosis of patients with CKD are also discussed.