Retrospective cohort study compares PTH control in hemodialysis with paricalcitol and calcitriol, suggesting no advantage.
Background/Objectives: Secondary hyperparathyroidism is a frequent component of chronic kidney disease-mineral and bone disorder in maintenance hemodialysis. Calcitriol and paricalcitol are used to suppress intact parathyroid hormone (iPTH), but the comparative advantage of paricalcitol in routine practice remains uncertain. This study compared 6-month biochemical PTH control in patients treated with intravenous calcitriol or intravenous paricalcitol. Methods: In this single-center retrospective cohort study, 312 adult hemodialysis patient files from 2023 to 2025 were screened. Patients who did not receive either intravenous study agent, switched between agents, or did not complete 6 months of treatment with the same agent were excluded. The final cohort included 185 patients, 100 treated with calcitriol and 85 with paricalcitol. The primary endpoint was target iPTH at 6 months, defined as 150–600 pg/mL. Results: Mean age was 58.9 ± 13.6 years, and 106 patients were male. Baseline iPTH was similar in the calcitriol and paricalcitol groups (684 ± 268 vs. 712 ± 291 pg/mL; p = 0.498). At 6 months, iPTH decreased significantly in both groups, with no significant between-group difference in follow-up iPTH (421 ± 214 vs. 398 ± 205 pg/mL; p = 0.456), percentage iPTH reduction (−36.8 ± 22.4% vs. −39.5 ± 24.1%; p = 0.431), or target iPTH achievement (62.0% vs. 60.0%; p = 0.781). Hypercalcemia and hyperphosphatemia rates were also similar. In multivariable analysis, treatment type was not independently associated with target iPTH achievement, whereas higher baseline iPTH and phosphorus were associated with lower odds of achieving target iPTH. Conclusions: Intravenous paricalcitol was not associated with superior 6-month PTH control compared with intravenous calcitriol in this real-world maintenance hemodialysis cohort. The findings indicate no demonstrated superiority of paricalcitol in this cohort and should not be interpreted as proof of pharmacological equivalence.
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Özdemir et al. (2026) studied this question.
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