Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation · 2003
Calcium-containing phosphate binder use associated with accelerated atherosclerotic coronary calcification.
Клинический случайСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Paret Cindy Lynch
Аннотация
OBJECTIVE: To report parameters and outcomes of phosphorus management in a maintenance hemodialysis patient who experienced atherosclerotic coronary calcification leading to myocardial infarction; to evaluate the role that high calcium intake over 6 years may have played in his coronary artery disease before the dangers of excess calcium intake in phosphorus management were recognized; and to describe an optimized therapeutic approach that provided improved mineral control.
DESIGN: Case study.
SETTING: A large outpatient in-center hemodialysis treatment unit.
MAIN OUTCOME MEASURES: Serum calcium, serum phosphorus, Ca x P product.
RESULTS: The year before his cardiac event, the patient's mean serum calcium was 9.6 mg/dL, mean serum phosphorus was 5.9 mg/dL, and mean Ca x P product was 57 mg2/dL2. Serum calcium peaked at 10.8 mg/dL shortly before his cardiac event. Treatment phases included high-dose calcium acetate (10 g Ca/day), low-dose calcium acetate (4 g Ca/day), low-dose calcium acetate plus low-dose sevelamer hydrochloride (4 g Ca/day plus 2.4 to 4.8 g sevelamer/day), and low-dose calcium acetate plus higher-dose sevelamer hydrochloride (4 g Ca/day plus 4.0 to 12.0 g sevelamer/day). With calcium acetate and sevelamer doses optimized, serum phosphorus levels and Ca x P products continued decreasing, with mean values of 5.99 mg/dL and 50.7 mg2/dL2, respectively, and serum calcium remained stable at a mean of 8.5 mg/dL. The patient has had no further myocardial infarctions.
CONCLUSIONS: This case illustrates how our growing understanding of phosphorus management and the addition of a calcium-free binder to our therapeutic armamentarium have improved phosphorus and calcium balance, reducing the risk of cardiovascular calcification.
DESIGN: Case study.
SETTING: A large outpatient in-center hemodialysis treatment unit.
MAIN OUTCOME MEASURES: Serum calcium, serum phosphorus, Ca x P product.
RESULTS: The year before his cardiac event, the patient's mean serum calcium was 9.6 mg/dL, mean serum phosphorus was 5.9 mg/dL, and mean Ca x P product was 57 mg2/dL2. Serum calcium peaked at 10.8 mg/dL shortly before his cardiac event. Treatment phases included high-dose calcium acetate (10 g Ca/day), low-dose calcium acetate (4 g Ca/day), low-dose calcium acetate plus low-dose sevelamer hydrochloride (4 g Ca/day plus 2.4 to 4.8 g sevelamer/day), and low-dose calcium acetate plus higher-dose sevelamer hydrochloride (4 g Ca/day plus 4.0 to 12.0 g sevelamer/day). With calcium acetate and sevelamer doses optimized, serum phosphorus levels and Ca x P products continued decreasing, with mean values of 5.99 mg/dL and 50.7 mg2/dL2, respectively, and serum calcium remained stable at a mean of 8.5 mg/dL. The patient has had no further myocardial infarctions.
CONCLUSIONS: This case illustrates how our growing understanding of phosphorus management and the addition of a calcium-free binder to our therapeutic armamentarium have improved phosphorus and calcium balance, reducing the risk of cardiovascular calcification.