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.

Calciphylaxis, also termed calcific uremic arteriolopathy, is a rare and devastating complication of end-stage renal disease (ESRD). Its occurrence in patients with HIV-associated ESRD is sparsely characterized in the literature. We report a 36-year-old African American woman with ESRD secondary to longstanding hypertension and virologically suppressed HIV infection (CD4 count 348 cells/μL) who developed three discrete presentations of recurrent calciphylaxis over 18 months, with histopathologic confirmation at initial diagnosis and at first recurrence. At initial presentation (T1), intact parathyroid hormone (iPTH) was 806.5 pg/mL; she was treated with paricalcitol, sevelamer carbonate, and intravenous sodium thiosulfate (STS) but remained intermittently nonadherent to hemodialysis and prescribed therapies, with a single-pool Kt/V of 0.29 documented at recurrence. At second presentation 12 months later (T2), iPTH was 308.4 pg/mL despite active cutaneous lesions; management included surgical debridement, broad-spectrum antibiotics for superimposed polymicrobial soft tissue infection, continued STS, and dialysis intensification. Six months after T2 (T3), the patient represented with lesion expansion and new ulcerations, and iPTH had risen to 1,764.9 pg/mL alongside hypocalcemia and hyperphosphatemia, consistent with progression toward tertiary hyperparathyroidism. Parathyroidectomy was deferred at T2 and T3 because of acute infectious burden and uncontrolled hyperkalemia, respectively. This case illustrates the diagnostic and management complexity of recurrent calciphylaxis in HIV-associated ESRD, demonstrates how intermittent treatment adherence may produce highly discordant iPTH measurements that complicate threshold-based monitoring, and underscores the importance of multidisciplinary planning before surgical and metabolic barriers to parathyroidectomy accumulate.

Vitamin D receptor (VDR) agonists promote quiescence of cancer-associated fibroblasts and improve efficacy of chemotherapy in preclinical models of pancreatic cancer. We conducted a run-in phase trial with primary endpoint of safety when the VDR agonist paricalcitol is given with first-line gemcitabine and albumin-bound paclitaxel (GA) in patients with metastatic pancreatic cancer. Secondary endpoints included pharmacodynamic analyses. Thirty-six patients were randomized to GA plus placebo, GA plus intravenous paricalcitol or GA plus oral paricalcitol with pretreatment and on-treatment tumor biopsies. Paricalcitol was safely administered with GA, although five patients (42%) receiving oral paricalcitol had grade 2-4 hypercalcemia and required dose reduction. Nuclear VDR protein expression was heterogeneous across patients, and VDR was expressed in tumor, immune and stromal cells. Compared to pretreatment specimens, on-treatment biopsies had decreased proportion of αSMA+ fibroblasts, altered fibroblast VDR activation signature and greater density and spatial colocalization of CD8+ T cells with tumor cells in the GA-plus-paricalcitol arms. VDR expression was predictive of tumor response in the GA-plus-paricalcitol arms. Paricalcitol can be safely administered with chemotherapy to patients with metastatic pancreatic cancer, and on-treatment biopsies indicated favorable modulation of the tumor microenvironment by paricalcitol as predicted by preclinical models. ClinicalTrials.gov identifier: NCT03520790 .