Cardiovascular calcification in patients with end-stage renal disease: a century-old phenomenon.
The mortality risk from cardiovascular disease is increased in patients with end-stage renal disease (ESRD). This is due to both traditional and dialysis-specific factors. Recently, a number of the dialysis-specific risk factors have been implicated in the pathogenesis of cardiovascular calcification. These include: hyperphosphatemia, high calcium-phosphate (Ca x P) product, elevated parathyroid hormone levels, duration of dialysis, and treatment with calcium-containing phosphate binders and vitamin D analogs. The recent availability of electron beam computed tomography (EBCT) has triggered increased awareness of the occurrence of cardiovascular calcification in ESRD patients. Given the development of transient hypercalcemia with calcium-containing binders, a link between calcium load from use of calcium-containing phosphate binders and development coronary calcification has been proposed. However, a causal relationship between use of these agents and cardiovascular calcification has not been established. Moreover, this phenomenon had been recognized over a century ago, long before these phosphate binders became available. Although its pathogenesis is likely to be multifactorial, available data strongly implicate elevated serum phosphorus as the primary culprit. Furthermore, the risk of calcification may be aggravated by vitamin D therapy, particularly in patients with severe secondary hyperparathyroidism. Therefore, achieving vigorous control of serum phosphorus, Ca x P product and parathyroid hormone level might decrease cardiovascular calcification and improve survival of patients on maintenance hemodialysis. Since calcium acetate is the most cost-effective phosphate binder available, we recommend that it should remain the first line treatment of hyperphosphatemia in patients with ESRD.
Qunibi
Wajeh Y
WY
Division of Nephrology, Department of Medicine, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, USA.
Nolan
Charles A
CA
Ayus
J Carlos
JC
D002114:Calcinosis / Q000209:etiology* / Q000266:history / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002614:Chelating Agents / Q000009:adverse effects; D003324:Coronary Artery Disease / Q000209:etiology* / Q000266:history / Q000378:metabolism; D003956:Dialysis / Q000009:adverse effects; D049673:History, 20th Century; D049674:History, 21st Century; D006801:Humans; D006934:Hypercalcemia / Q000150:complications; D054559:Hyperphosphatemia / Q000150:complications* / Q000188:drug therapy / Q000209:etiology / Q000266:history; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000266:history / Q000378:metabolism / Q000628:therapy; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D010281:Parathyroid Hormone / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism; D012307:Risk Factors; D014807:Vitamin D / Q000009:adverse effects / Q000031:analogs & derivatives; D014815:Vitamins / Q000009:adverse effects
D002614:Chelating Agents; D010281:Parathyroid Hormone; D014815:Vitamins; D014807:Vitamin D; D010758:Phosphorus; D002118:Calcium