Secondary hyperparathyroidism (SHPT) is common in chronic kidney disease (CKD) patients. Classically, SHPT is induced by hypocalcemia, hyperphosphatemia, and calcitriol deficiency, that cause not only renal osteodystrophy but also systemic toxicity, particularly cardiovascular disease. Treatment with calcitriol, the active form of vitamin D, reduces serum parathyroid hormone (PTH) levels but may result in both hypercalcemia and hyperphosphatemia, increasing the risk of vascular calcification in CKD. Are the new vitamin D receptor activators (VDRAs) more useful in the treatment of SHPT for their reduced risk of hypercalcemia and hyperphosphatemia in haemodialysis (HD) patients? In this review, we describe the new VDRA, paricalcitol (1,25-dihydroxy-19-nor-vitamin D2), which suppresses PTH secretion with minimal increases on serum calcium and phosphate levels. In some animal models of CKD paricalcitol does not cause vascular calcification, while other VDRAs do. These data may account for the results seen in observational studies of HD patients, in which paricalcitol is associated with improved survival compared to calcitriol.
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