Background: In dialysis patients, non-adherence to oral cinacalcet adds complexity to the control of secondary hyperparathyroidism. The present study aims to evaluate the use of intravenous calcimimetic, etelcalcetide, in the control of secondary hyperparathyroidism in patients adherent and non-adherent to oral calcimimetics.
Method: The Simplified Medication Adherence Questionnaire was used to identify non-adherence. Almost half of the patients were non-adherent to the treatment with cinacalcet. Twenty-five patients (15 non-adherent) were switched from cinacalcet to etelcalcetide and were followed-up monthly for 8 months.
Results: Cinacalcet was discontinued for 1 week before the initiation of etelcalcetide. After this period, the serum PTH levels increased by2-fold in adherent patients, whereas it did not change in non-adherent patients suggesting that they were not taking the medication. Etelcalcetide progressively reduced serum parathyroid hormone (PTH) (mean ± standard deviation) from 818 ± 395 to 367 ± 289 pg/mL (P<0.001) in non-adherents, and from 496 ± 172 to 228 ± 111 pg/mL (P<0.01) in adherent patients with a mean dose of 7.0 ± 2.3 and 5.1 ± 1.2 mg in non-adherent and in adherent patients, respectively. Etelcalcetide increased the percentage of patients with PTH on target from 28% to 58%. Patients with serum calcium <8.4 mg/dL increased from 8% to 40%, although they remained asymptomatic. The percent of patients with serum phosphate on target increased from 40% to 65%.
Conclusion: The lack of adherence to cinacalcet is a possible cause of the apparent lack of response to oral calcimimetic. The use of etelcalcetide ensures compliance and control of secondary hyperparathyroidism in both non-adherent and adherent patients.
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http://dx.doi.org/10.1093/ckj/sfaa005 | DOI Listing |
Naunyn Schmiedebergs Arch Pharmacol
December 2024
Xiangya School of Pharmacy, Central South University, Changsha, 410013, Hunan, China.
This study aimed to evaluate the pharmacokinetics (PK), pharmacodynamics (PD), safety, and tolerability of SHR6508 injection, a new calcimimetic agent, in healthy Chinese subjects following single dose. This study utilized a placebo-controlled, single-dose, and dose-escalation design with four dose groups (0.5 mg, 2.
View Article and Find Full Text PDFNephrology (Carlton)
January 2025
Kwong Wah Hospital, Kowloon, Hong Kong.
Post-transplant hyperparathyroidism (PT-HPT) is common in kidney transplant recipients (KTRs) and can cause nephrocalcinosis and graft dysfunction. Cinacalcet is commonly used for treating PT-HPT but may induce calciuria and exacerbate nephrocalcinosis. The concurrent use of bisphosphonates with cinacalcet to prevent this complication has not been reported.
View Article and Find Full Text PDFTher Apher Dial
November 2024
Instituto de Diagnostico e Investigaciones Metabólicas (IDIM), Buenos Aires, Argentina.
Introduction: Secondary hyperparathyroidism (sHPT) is a common complication in patients with chronic kidney disease (CKD). Recently, etelcalcetide (EC), an intravenous calcimimetic, has been introduced as a treatment. We evaluated the efficacy of EC in treating sHPT.
View Article and Find Full Text PDFInt J Biol Macromol
September 2024
TMU Research Center of Urology and Kidney, Taipei Medical University, Taipei, Taiwan; Division of Nephrology, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Division of Nephrology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan. Electronic address:
Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a multifaceted clinical syndrome characterized by mineral imbalances, abnormalities in bone metabolism, chronic inflammation and vascular calcification. Etelcalcetide, a second-generation intravenous calcimimetic agent, has been approved for treating high-turnover renal osteodystrophy, effectively targeting the pathophysiological mechanisms underlying this condition. We investigate the impacts of etelcalcetide on osteoclast (OC) differentiation and functionality in CKD-MBD via three critical mechanisms: inflammation initiated by interferon regulatory factor 7 (IRF7), receptor-interacting protein (RIP)-mediated necroptosis and apoptosis-induced cell death.
View Article and Find Full Text PDFPediatr Endocrinol Diabetes Metab
July 2024
Research Centre, King Faisal Specialist Hospital & Research Centre, Saudi Arabia.
Introduction: Hereditary vitamin D resistant rickets (HVDRR) is a rare autosomal recessive disorder marked by end-organ resistance of 1,25-dihydroxyvitamin D secondary to various mutations in the vitamin D receptor gene. The currently accepted treatment modality involves bypassing the affected receptors in the gut with high-dose intravenous calcium. In a few limited case reports, cinacalcet, a calcimimetic, has been used as an adjunctive therapy.
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