Vitamin D homeostasis is known to be altered in persons with chronic kidney disease (CKD). Both reductions of vitamin D activation and catabolism are prominent features of the CKD–mineral and bone disorder (MBD).1 The classical understanding of these processes involved a loss of nephron mass resulting in a loss of CYP27B1 (the enzyme that converts 25(OH) vitamin D to the active 1,25(OH)2 vitamin D hormone or calcitriol), leading to a loss of calcitriol production, and a resultant disinhibition of the parathyroid hormone (PTH), and secondary hyperparathyroidism.