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Cholecalciferol Supplementation Alters Calcitriol-Responsive Monocyte Proteins and Decreases Inflammatory Cytokines in ESRD

Jason R. Stubbs^*, Arun Idiculla^*, Joyce Slusser, Rochelle Menard^* and L. Darryl Quarles^*

*The Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas; and
Flow Cytometry Core Laboratory, University of Kansas Medical Center, Kansas City, Kansas

Correspondence: Dr. Jason R. Stubbs, 3901 Rainbow Boulevard, MS 3002, Kansas City, KS 66160. Phone: 913-588-6074; Fax: 913-588-3867; E-mail: jstubbs{at}kumc.edu

Received for publication April 28, 2009. Accepted for publication September 24, 2009.

In vitro, monocyte 1-hydroxylase converts 25-hydroxyvitamin D [25(OH)D] to 1,25-dihydroxyvitamin D to regulate local innate immune responses, but whether 25(OH)D repletion affects vitamin D–responsive monocyte pathways in vivo is unknown. Here, we identified seven patients who had 25(OH)D insufficiency and were undergoing long-term hemodialysis and assessed changes after cholecalciferol and paricalcitol therapies in both vitamin D–responsive proteins in circulating monocytes and serum levels of inflammatory cytokines. Cholecalciferol therapy increased serum 25(OH)D levels four-fold, monocyte vitamin D receptor expression three-fold, and 24-hydroxylase expression; therapy decreased monocyte 1-hydroxylase levels. The CD16⁺ "inflammatory" monocyte subset responded to 25(OH)D repletion the most, demonstrating the greatest increase in vitamin D receptor expression after cholecalciferol. Cholecalciferol therapy reduced circulating levels of inflammatory cytokines, including IL-8, IL-6, and TNF. These data suggest that nutritional vitamin D therapy has a biologic effect on circulating monocytes and associated inflammatory markers in patients with ESRD.

Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673