title: Management of vascular calcification in CKD patients.
abstract: Vascular calcification is common in patients with chronic kidney disease (CKD) and it may affect almost every artery. It is associated with a significant increase in morbidity and mortality. Therefore, the detection, prevention and treatment of vascular calcification in CKD patients are critical for the overall approach for the management of these patients. Hyperphosphatemia, especially when the blood levels of serum phosphorus are above 5.5 mg/dl, plays a major role in the development of vascular calcification. Hyperphosphatemia induces vascular calcification by both passive and active processes. By increasing calcium-phosphate product, hyperphosphatemia results in direct deposition of calcium salts in the arteries and in cardiac valves. The active process involves the uptake of phosphate by the smooth muscle cells of the arteries by a Na-P co-transporter. This increase in cell phosphate then induces phenotypic changes of these cells, rendering them into osteoblasts which in turn, begin laying calcium salts in the arterial walls. Therefore, it is critical that the blood levels of serum phosphorus be maintained below 5.5 mg/dl in CKD patients. Inflammation and the production of C-reactive protein (CRP) and interleukin 6 are also risk factors for vascular injury and vascular calcification. In a study of 254 dialysis patients with elevated blood levels of CRP (>1.0 mg/l) and 258 patients with CRP levels equal to or less than 1.0 mg/l, it was found that higher levels of CRP are significantly associated with the presence of both atheromatous and medial calcification of the aorta and hand arteries. Also, it was reported that a significant association between CRP levels and cardiac valves calcification in patients undergoing continuous ambulatory peritoneal dialysis. The reasons for the elevation in CRP in dialysis patients are not clear, but certainly, is more evident in those with obvious inflammatory processes. Therefore, any inflammation that is detected should be treated appropriately.
authors.affiliation: Division of Nephrology and the Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. massry@usc.edu
authors.forename: Shaul G
authors.initials: SG
authors.lastname: Massry
authors.forename: Miroslaw
authors.initials: M
authors.lastname: Smogorzewski
mesh_terms: D002114:Calcinosis / Q000209:etiology* / Q000628:therapy*; D002908:Chronic Disease; D006801:Humans; D007674:Kidney Diseases / Q000150:complications*; D010760:Phosphorus Metabolism Disorders / Q000150:complications / Q000628:therapy; D014652:Vascular Diseases / Q000209:etiology* / Q000628:therapy*