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Cardiovascular calcification in patients with end-stage renal disease: a century-old phenomenon
Wajeh Y Qunibi1, Charles A Nolan, J Carlos Ayus
1Division of Nephrology, Department of Medicine, University of Texas Health Sciences Center at San Antonio, San Antonio, Texas, USA.
Insights
Patients with end-stage renal disease (ESRD) face high cardiovascular disease risk. Controlling phosphorus, calcium-phosphate product, and parathyroid hormone levels may reduce cardiovascular calcification and improve survival.
Area of Science:
- Nephrology
- Cardiology
- Biochemistry
Background:
- Cardiovascular disease (CVD) mortality is elevated in end-stage renal disease (ESRD) patients.
- Dialysis-specific factors contribute to CVD risk, including cardiovascular calcification.
- Risk factors include hyperphosphatemia, high calcium-phosphate product, and elevated parathyroid hormone.
Observation:
- Electron beam computed tomography (EBCT) highlights cardiovascular calcification in ESRD.
- Calcium-containing phosphate binders have been linked to coronary calcification, though causality is unproven.
- Cardiovascular calcification predates modern phosphate binders.
Findings:
- Elevated serum phosphorus is strongly implicated as the primary cause of cardiovascular calcification.
- Vitamin D therapy may exacerbate calcification risk, especially with secondary hyperparathyroidism.
- Controlling phosphorus, Ca x P product, and PTH is crucial for reducing calcification.
Implications:
- Vigorous control of key biochemical markers may decrease cardiovascular calcification.
- Improved management could enhance survival rates for patients on maintenance hemodialysis.
- Calcium acetate is recommended as a cost-effective first-line treatment for hyperphosphatemia in ESRD.
Abstract:
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.