Abstract
The introduction of less-calcemic vitamin D analogs in 1998 was the beginning of a fundamental change in the management paradigm for secondary hyperparathyroidism in patients with chronic kidney disease (1). Until that time, the prevailing treatment strategy involved maintaining serum calcium (Ca) at the upper limit of normal to facilitate calcium-induced suppression of parathyroid hormone (PTH) synthesis and secretion. The inevitable transient episodes of hypercalcemia were viewed as a clinical management “nuisance” requiring temporary interruption of vitamin D therapy. Concurrent with the availability of this new therapeutic agent, which suggested the promise of having fewer episodes of hypercalcemia, observational evidence emerged, which suggested that patients with a lower calcium × phosphorus (P) product (Ca × P), lower serum Ca, and lower serum P had a survival advantage as compared with those with higher serum levels of these ions (2,3). There have been a number of distinct data sets examining the relationship between serum Ca and clinical outcomes. Data from a large dialysis chain in the …
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