Thirty-Month Follow-Up of Coronary Artery Calcification in Hemodialysis Patients: Different Roles for Inflammation and Abnormal Calcium-Phosphorous Metabolism?

• Published in: Renal failure Vol. 29; no. 5; pp. 623 - 629
• Main Authors: Patsalas, Stavros, Eleftheriadis, Theodoros, Spaia, Sofia, Theodoroglou, Hariklia, Antoniadi, Georgia, Liakopoulos, Vassilis, Passadakis, Ploumis, Vayonas, Georgios, Vargemezis, Vassilis
• Format: Journal Article
• Language: English
• Published: Colchester Informa UK Ltd 01.01.2007; Taylor & Francis
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Calcinosis - etiology; Calcium Metabolism Disorders - complications; coronary calcification; Coronary Disease - etiology; Disease Progression; Emergency and intensive care: renal failure. Dialysis management; Female; Follow-Up Studies; hemodialysis; Humans; inflammation; Inflammation - complications; Intensive care medicine; Male; Medical sciences; Middle Aged; Nephrology. Urinary tract diseases; phosphorous; Phosphorus Metabolism Disorders - complications; Renal Dialysis - adverse effects; Risk Factors; Time Factors; Human; Nephrology; Calcium; Hemodialysis; Coronary artery; Cardiovascular disease; Inflammation; Metabolism; Inorganic element; Coronary heart disease; phosphorous; Extrarenal dialysis; coronary calcification; Calcification; Anesthesia; Resuscitation
• ISSN: 0886-022X; 1525-6049
• DOI: 10.1080/08860220701395010

Background. Cardiovascular disease is the leading cause of death in hemodialysis (HD) patients. Coronary artery calcification (CAC) is considered a marker of atherosclerosis and coronary artery disease (CAD). The CAC progression and factors that influence it were evaluated during a 30-month period. Methods. Forty HD patients without a history of CAD were enrolled into the study. CAC score was assessed with conventional CT repeated every six months. The circulating factors of phosphorous, calcium, calcium-phosphorous product, intact parathyroid hormone, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, lipoprotein-alpha, albumin, high sensitivity C-reactive protein, and fibrinogen were measured monthly. Hypertension and calcium intake during the study period were taken into account as well. Results. At baseline, CAC score was correlated with age and duration of HD therapy. From all evaluated factors, CAC initiation was influenced only by older age and C-reactive protein. CAC, when it was started, was aggravated continuously and was influenced only by elevated serum phosphorous and calcium-phosphorous product. Hypertension, lipid profile, and calcium intake did not affect CAC initiation or progression. Conclusions. Once CAC progression starts, it is an uninterrupted process. The roles of inflammation and abnormal calcium-phosphorous metabolism in CAC differ. Inflammation is the major factor that contributes in CAC initiation. Elevated serum phosphorous and calcium-phosphorous product accelerates CAC progression.