Study: Vitamin D agents deemed similar for treating coronary artery calcification in CKD
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Researchers found no difference in coronary artery calcification progression between patients with chronic kidney disease and secondary hyperparathyroidism who were randomized to either calcitriol or paricalcitol.
“Mineral and bone disorder [MBD] in chronic kidney disease (CKD) is associated with progression of coronary artery calcification (CAC),” Karim H. Anis, MD, of Joslin Diabetes Center at Harvard Medical School, and colleagues. “Mineral and bone disorder often is treated with calcitriol and other vitamin D receptor activators, including paricalcitol, agents that may have differential effects on calcium, phosphorus and parathyroid hormone (PTH) levels.”
According to the researchers, calcitriol and paricalcitol have both demonstrated effectiveness in reducing parathyroid hormone levels by inhibiting PTH synthesis and secretion. Further, they contended that the paricalcitol dose needed to produce the same level of hypercalcemia is approximately 10 times that of calcitriol, and that “paricalcitol is at least as potent as calcitriol in decreasing serum PTH, while reportedly causing less vascular calcification in animal studies.”
The researchers sought to investigate the differential effects of oral calcitriol and paricalcitol on CAC on this patient population, noting that the 2009 Kidney Disease Improving Global Outcomes CKD-MBD guidelines discussed a lack of consensus on vitamin D analogs for the treatment of vascular calcification in patients with CKD and secondary hyperparathyroidism.
Hypothesizing that patients treated with paricalcitol would have a slower progression of CAC compared to those treated with calcitriol (based on previous in vivo animal data), Anis and colleagues randomly assigned 44 adults with any CAC score of greater than zero (median baseline CAC score, 140 Agatston units) to each of the treatment groups. Those randomized to calcitriol initiated treatment at 0.25 mcg three times a week, with an increase to 0.5 mcg three times per week if PTH was not at goal at 12 weeks. For those taking paricalcitol, the starting dose was 2 mcg three times per week, which was titrated up during the next visit according to PTH levels. If PTH levels were not at goal by 12 weeks, paricalcitol was also increased (4 mcg three times per week).
All patients had never been treated previously with activated vitamin D.
The annualized percent change in CAC for all patients was 32.2%.
After 48 weeks, researchers found no significant difference in CAC progression between treatment groups. This remained true after adjustments for baseline CAC score, creatinine level and CKD stage.
Progression of cardiac valve calcification was also not different between the two groups.
Further observations demonstrated an interaction between higher dose of treatment and CAC progression.
The researchers addressed some limitations to the study, including that the results are not generalizable to patients on dialysis (as only those with CKD stages 3 and 4 were included).
In addition, they wrote, “there is no placebo group because the majority of the patients had already been assigned to start activated vitamin D therapy by their providers ... Our pilot study provides support for an appropriately powered placebo control trial of activated vitamin D therapy in individuals with CKD.”
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