What are the nonsurgical treatment options for secondary hyperparathyroidism?

Updated: Dec 24, 2020
  • Author: Lawrence T Kim, MD, FACS, FACE; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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The following is a list of current nonsurgical treatment options for management of secondary hyperparathyroidism in CKD:    

  • Dietary phosphorus restriction may be initiated if parathyroid hormone is elevated despite sufficient 25-hydroxyvitamin D (>20 ng/mL).
  • Phosphate binders may be considered if hyperphosphatemia persists despite dietary phosphate restriction. These include calcium-based phosphate binders such as calcium carbonate or calcium acetate and non–calcium-based phosphate binders such as sevelamer hydrochloride, lanthanum carbonate, ferric citrate, or sucroferric oxyhydroxide.
  • Non–calcium-based binders are generally preferred for use over calcium-based binders due to concern that excess calcium supplementation may increase coronary artery calcification and cardiovascular risk. [57]  
  • Vitamin D and its analogs may be used—including calcitriol and analogs of calcitriol such as calcifediol, paricalcitol, doxercalciferol, maxacalcitol, and falecalcitriol—to treat hypocalcemia and secondary hyperparathyroidism. [58]  Treatment with calcimimetics such as cinacalcet leads to significant improvements in biochemical parameters, but patient-based benefits have not yet been demonstrated.
  • The newest class of drugs to reduce the parathyroid hormone level, the aforementioned calcimimetics—which includes etelcalcetide (Parsabiv) and cinacalcet (Sensipar)—binds to and activates the calcium-sensing receptor. Activation of this receptor on parathyroid chief cells decreases parathyroid hormone secretion. Etelcalcetide can be administered intravenously at the end of hemodialysis sessions. Its approval was based on randomized, double-blind trials that compared the drug to placebo and cinacalcet. Patients in both studies were on hemodialysis and had moderate to severe secondary hyperparathyroidism. Those taking etelcalcetide had a significantly greater chance of reaching the primary efficacy endpoint (>30% reduction from baseline in mean predialysis parathyroid concentration at 20-27 weeks) than did patients receiving placebo (74-75.3% vs 8.3-9.6%, respectively). [53] When compared with cinacalcet, etelcalcetide was superior in decreasing parathyroid hormone levels over the span of 26 weeks. [59]
  • The EVOLVE (EValuation Of Cinacalcet HCl Therapy to Lower CardioVascular Events) trial was one of the first large-scale, randomized controlled trials in patients with ESRD to examine the treatment of secondary hyperparathyroidism with cinacalcet vs placebo along with standard of care phosphorous binders and vitamin D analogs. Hyperphosphatemia and hyperparathyroidism have been associated with increased risk of death in ESRD patients and this trial was designed to see if there was a mortality benefit in the use of the noncalcium/non–vitamin D analog cinacalcet in the ESRD population. The results of the trial demonstrated that cinacalcet did not result in improved mortality or improve cardiovascular endpoints. The use of cinacalcet did reduce the need for parathyroidectomy for refractory hyperparathyroidism. Of note, there was an increased risk of serious adverse events, namely hypocalcemia, with the use of cinacalcet. In conclusion, despite aggressive management of secondary hyperparathyroidism that is associated with increased mortality in ESRD patients, cinacalcet did not offer a cardiovascular or mortality benefit in this population of patients. [60]

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