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Animal studies suggest that calcium-phosphorus homeostatic abnormalities cause cardiovascular disease in uremia; few observational studies in humans have explored this. Associations in the retrospective United States Renal Data System Waves 1, 3, and 4 Study of 14,829 patients who were on hemodialysis on December 31, 1993, were examined. Mean age and duration of renal replacement therapy were 60.0 and 3.2 yr, respectively; 40.7% had diabetes. Quintiles (Q(1) to Q(5)) of (albumin-adjusted) calcium were 10.2 mg/dl; phosphorus, 7.5 mg/dl; calcium-phosphorus product, 71.0 mg(2)/dl(2); and parathyroid hormone (PTH), 480 pg/ml. Higher calcium levels were associated with fatal or nonfatal cardiovascular events (adjusted hazards ratio, 1.08 for Q(5), versus Q(1)) and all-cause mortality (Q(2), 1.07; Q(4), 1.11; Q(5), 1.14). Phosphorus levels were associated with cardiovascular events (Q(2), 1.06; Q(3), 1.13; Q(4), 1.14; Q(5), 1.25) and mortality (Q(4), 1.10; Q(5), 1.19), calcium-phosphorus product was associated with cardiovascular events (Q(3), 1.09; Q(4), 1.14; Q(5), 1.24) and mortality (Q(4), 1.09; Q(5), 1.19), and PTH levels were associated with cardiovascular events (Q(5), 1.12) and mortality (Q(5), 1.17). Despite limitations (including retrospective design; noncurrent study era; and lack of serial calcium, phosphorus, and PTH measurements), this study suggests that disorders of calcium homeostasis are associated with fatal and nonfatal cardiovascular events and all-cause mortality in hemodialysis patients.
Slinin et al. (Thu,) studied this question.