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Background <p>Hemodialysis (HD) patients lose renal CYP27B1 (cytochrome P450 25-hydroxyvitamin D-1α-hydroxylase) as kidney function declines causing low serum total 25-hydroxyvitamin D (25D) and 1,25-dihydroxyvitamin D (1,25D), and elevated intact parathyroid hormone (iPTH). Most require vitamin D hormone treatment which increases the risk of hypercalcemia. A recent randomized controlled trial (RCT) in HD patients showed that extended-release calcifediol (ERC) could safely raise serum 25D to high levels (≥ 50 ng/mL) and drive sufficient alternative production of 1,25D by extra-renal CYP27B1, potentially avoiding the need for hormone treatment.</p> Case presentation <p>A 41-year-old Caucasian male requiring regular HD was overdosed with 900 (rather than 300) µg/HD of ERC for 10 weeks in the RCT referenced above. When the overdosing was recognized, serum 25D had increased 18-fold (from 19 to 339 ng/mL), 1,25D had risen 23-fold (from 6 to 137 pg/mL), and iPTH had decreased 67% (from 440 to 146 pg/mL) with no impact on calcium, phosphorus or treatment-emergent adverse events noted.</p> Conclusions <p>The observations from this case report are consistent with the conclusion from the full RCT with ERC in HD patients that serum 25D repletion can control elevated iPTH in advanced chronic kidney disease by supporting adequate extra-renal 1,25D production. They also indicate that serum 25D levels required for adequate extra-renal 1,25D production and effective iPTH control are much higher than commonly used repletion targets of 20 or 30 ng/mL, and published estimates of serum 25D toxicity thresholds are probably too low for ERC. These observations, however, require substantiation in further clinical trials with ERC in end-stage kidney disease patients.</p>

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High-dose extended-release calcifediol successfully treated advanced secondary hyperparathyroidism in an end-stage kidney disease patient: a case report

  • 期刊论文

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  • 发表日期：

    2025年8月7日

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  • Akhtar Ashfaq,
  • John Choe,
  • Samir Tabash,
  • Stephen A. Strugnell,
  • Laura L. Johnson,
  • Charles W. Bishop

摘要

Background

Hemodialysis (HD) patients lose renal CYP27B1 (cytochrome P450 25-hydroxyvitamin D-1α-hydroxylase) as kidney function declines causing low serum total 25-hydroxyvitamin D (25D) and 1,25-dihydroxyvitamin D (1,25D), and elevated intact parathyroid hormone (iPTH). Most require vitamin D hormone treatment which increases the risk of hypercalcemia. A recent randomized controlled trial (RCT) in HD patients showed that extended-release calcifediol (ERC) could safely raise serum 25D to high levels (≥ 50 ng/mL) and drive sufficient alternative production of 1,25D by extra-renal CYP27B1, potentially avoiding the need for hormone treatment.

Case presentation

A 41-year-old Caucasian male requiring regular HD was overdosed with 900 (rather than 300) µg/HD of ERC for 10 weeks in the RCT referenced above. When the overdosing was recognized, serum 25D had increased 18-fold (from 19 to 339 ng/mL), 1,25D had risen 23-fold (from 6 to 137 pg/mL), and iPTH had decreased 67% (from 440 to 146 pg/mL) with no impact on calcium, phosphorus or treatment-emergent adverse events noted.

Conclusions

The observations from this case report are consistent with the conclusion from the full RCT with ERC in HD patients that serum 25D repletion can control elevated iPTH in advanced chronic kidney disease by supporting adequate extra-renal 1,25D production. They also indicate that serum 25D levels required for adequate extra-renal 1,25D production and effective iPTH control are much higher than commonly used repletion targets of 20 or 30 ng/mL, and published estimates of serum 25D toxicity thresholds are probably too low for ERC. These observations, however, require substantiation in further clinical trials with ERC in end-stage kidney disease patients.