The assumption has been that 1,25(OH)2D is solely responsible for calcium absorption. That has been one of the presumed causes of hyperparathyroidism in chronic kidney disease (CKD) (low 1,25(OH)2D leads to decreased calcium absorption, which increases parathyroid hormone release in compensation). Replacing 1,25 D directly has been the goal with using 1,25D or its analogues in CKD. There is very little data concerning use of native vitamin D or 25(OH)D in CKD, although autocrine functions in extrarenal tissues would use 25(OH)D. The latest KDIGO guidelines do recognize the autocrine role of vitamin D, but have no data on outcomes or doses or optimal levels to guide them and so have made a blanket recommendation to treat 25D levels in CKD by general healthy population guidelines.

1. This project focuses on an outcome (calcium absorption) that may be impacted by optimizing 25D status in renal patients. The investigators will assume for this project that a level of 25D > 32 ng/ml is optimal in CKD patients as in a healthy population.
2. A secondary outcome is to quantify calcium absorption in CKD patients with and without vitamin D repletion and to quantify systemic 1,25D levels. This may clarify the roles 25D and 1,25D play in calcium absorption.

Inclusion Criteria:

• on hemodialysis
• > 19 years of age

Exclusion Criteria:

• Pregnancy or planned pregnancy
• Hypercalcemia (> 10.2 mg/dl) at baseline
• Chronic GI disease
• Liver dysfunction
• Taking steroids
• Received any investigational drugs within 4 weeks
• Any allergy to vitamin D3
• Chronic vitamin D intake > 1,000 IU daily
• Dialysate concentration (calcium 2.5mg/L) which is to remain constant during Rx