ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: FR-PO274

Effects of Acute Administration of Ergocalciferol on Vitamin D Catabolism in Hemodialysis Patients

Session Information

Category: Mineral Disease

  • 1202 Mineral Disease: Vitamin D, PTH, FGF-23

Authors

  • Sirimongkolchaiyakul, Ornatcha, David Geffen School of Medicine at UCLA, Los Angeles, California, United States
  • Berg, Anders H., None, Boston, Massachusetts, United States
  • Karumanchi, S. Ananth, Beth Israel Deaconess Medical Ctr/Harvard Medical School, Boston, Massachusetts, United States
  • Wesseling-Perry, Katherine, David Geffen School of Medicine at UCLA, Los Angeles, California, United States
  • Thadhani, Ravi I., Massachusetts General Hospital, Boston, Massachusetts, United States
  • Salusky, Isidro B., Mattel Children's Hospital, Los Angeles, California, United States
Background

Vitamin D deficiency is highly prevalent in dialysis patients and D supplementation has been recommended. However, there is limited data of vitamin D catabolism in advanced CKD. Stimulation of 24-hydroxylase mediated catabolism of vitamin D metabolites may reduce serum 25(OH)D and 1, 25(OH)2D levels. To test this possibility, we assessed vitamin D catabolism after a single ergocalciferol administration (D2) in hemodialysis patients (HD) and healthy volunteers (HV).

Methods

All subjects ingested a single oral dose of 50,000 IU ergocalciferol, HD patients aged 65.8 (20.6, 71.0) years (n = 35) and HV aged 41.0 (29.0, 62.0) years (n = 7). Biochemical determinations of 25D, 1,25D, 24,25 D and DBP were measured at baseline and 2-5 days after D2 ingestion. Biochemical markers at baseline and post-therapy were compared.

Results

Concentrations of 25D2 increased after D2 in both HD and HV (average increases of +14.5 ng/mL [95%CI 9.5-29.4] and +21.2 [95%CI 14.6-29.8], respectively). Although average pre-treatment 25D3 concentrations were significantly higher in HD compared to HV (21.2 ng/mL [95% CI 14.6-29.8] vs. 14.5 ng/mL [95%CI 9.5-29.4], p<0.05), concentrations of 24,25D3 were lower in HD (5.5 ng/mL [95% CI 3.5-15.6] vs. 14.5 ng/mL [95%CI 9.5-29.4], p<0.05). Average concentrations of 1,25D3 was also lower in HD (4.7 pg/mL [95% CI 2.8-8.4] vs. 54.1 pg/mL [95%CI 47.7-69.2], p<0.05). Amongst HV, concentrations of 25D3 decreased on average by -0.6 ng/mL [95%CI -3.9 to -0.2] after Vitamin D2 administration, and 1,25D3 decreased by -10.6 pg/mL(95%CI -20.2 to -0.5), whereas there was no significant decrease in 24,25D3. Amongst HD, no significant changes in 25D3, 24,25D3, or 1,25D3 were seen. Amongst HV, concentrations of both 1,25D3 and 24,25D3 correlated strongly with 25D3 (R2 = 0.4558 and R2 = 0.6993, respectively). In contrast, the correlations between 25D3 and 1,25D3 and between 25D3 and 24,25D3 in HD were weaker (R2 = 0.1285 and R2 = 0.4654, respectively).

Conclusion

CKD is associated with higher 25D3 but lower 24,25D and 1,25D concentrations, and 1,25 levels are more closely associated with 24,25D than with 25D in ESKD. Feedback regulation of both 1,25D and 24,25D by PTH and/or FGF23 in HD warrants further investigation.

Funding

  • NIDDK Support