Dysregulated mineral metabolism in patients with acute kidney injury and risk of adverse outcomes
Article first published online: 26 MAR 2013
© 2013 John Wiley & Sons Ltd
Volume 79, Issue 4, pages 491–498, October 2013
How to Cite
Leaf, D. E., Waikar, S. S., Wolf, M., Cremers, S., Bhan, I. and Stern, L. (2013), Dysregulated mineral metabolism in patients with acute kidney injury and risk of adverse outcomes. Clinical Endocrinology, 79: 491–498. doi: 10.1111/cen.12172
- Issue published online: 5 SEP 2013
- Article first published online: 26 MAR 2013
- Accepted manuscript online: 18 FEB 2013 03:17AM EST
- Manuscript Accepted: 10 FEB 2013
- Manuscript Revised: 7 JAN 2013
- Manuscript Revised: 16 DEC 2012
- Manuscript Received: 16 NOV 2012
- generous donation from the Nortillo Foundation
- Columbia University Clinical and Translational Science Award. Grant Number: UL1RR024156
- National Center for Research Resources/National Institutes of Health
- National Institutes of Health. Grant Numbers: R01DK076116, R01DK081374
Numerous studies have evaluated the prevalence and importance of vitamin D deficiency among patients with chronic kidney disease and end-stage renal disease; however, little is known about vitamin D levels in acute kidney injury (AKI). We evaluated the association between vitamin D metabolites and clinical outcomes among patients with AKI.
Prospective cohort study.
A total of 30 participants with AKI and 30 controls from general hospital wards and intensive care units at a tertiary care hospital were recruited for the study.
Plasma levels of 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1,25(OH)2D], 24R,25-dihydroxyvitamin D3, vitamin D binding protein (VDBP) and fibroblast growth factor 23 (FGF23) were measured within 24 hours of AKI onset and 5 days later. Bioavailable 25(OH)D and 1,25(OH)2D levels, defined as the sum of free- and albumin-bound 25(OH)D and 1,25(OH)2D, were estimated using equations.
Compared to controls, participants with AKI had lower levels of 1,25(OH)2D [17 (10–22) vs 25 (15–35) pg/ml, P = 0·01], lower levels of VDBP [23 (15-31) vs 29 (25–36) mg/dl, P = 0·003] and similar levels of bioavailable 25(OH)D and 1,25(OH)2D at enrolment. Levels of bioavailable 25(OH)D were inversely associated with severity of sepsis in the overall sample (P < 0·001). Among participants with AKI, bioavailable 25(OH)D, but not other vitamin D metabolites, was significantly associated with mortality after adjusting for age and serum creatinine (adjusted odds ratio per 1 SD ln [bioavailable 25(OH)D] = 0·16, 95% confidence interval = 0·03–0·85).
Bioavailable 25(OH)D could have a role as a biomarker or mediator of adverse outcomes among patients with established AKI.