Effect of Ergocalciferol on Iron Metabolism in Individuals With Chronic Kidney Disease

Targeting the Interactions Between Disordered Iron Homeostasis and Mineral Metabolism in Chronic Kidney Disease (Aim 1)

The purpose of the study is to learn more about how treatment with vitamin D can affect iron metabolism and blood levels of hepcidin (hormone controlling iron levels) in people with chronic kidney disease (CKD).

Iron is an essential mineral which is a major component of proteins that carry oxygen in the blood. Problems with iron metabolism can lead to low blood levels (anemia), which can commonly happen in people with CKD.

New research over the last decade has uncovered a new hormone called 'hepcidin', which is made in the liver and released into the blood. Hepcidin controls how much iron is in the blood by preventing the absorption of iron from food. Blood levels of hepcidin C are found to be high in people with CKD, and a recent small study in people with normal kidney function showed that treatment with vitamin D decreased hepcidin levels.

In this study, investigators would like to examine the effects of vitamin D (Ergocalciferol) on iron metabolism and blood levels of hepcidin in individuals with CKD.

Inclusion Criteria:

• Participants 19 years or older with mild to moderate CKD (eGFR 15 - 59 ml/min/1.73 m2) by the CKD-EPI formula, with vitamin D deficiency (25(OH)D < 30 ng/ml), and with absolute iron deficiency (TSAT < 20 and Ferritin <100) or iron restriction (TSAT < 20 and Ferritin > 100).

Exclusion Criteria:

• Active vitamin D analog therapy or history of recent (< 3 months) use.
• Nutritional vitamin D (cholecalciferol or ergocalciferol) therapy in dosages greater than 2000 IU/day.
• Subjects receiving erythropoiesis stimulating agents or intravenous iron therapy.
• Oral iron therapy started within the last 3 months.
• Hb < 8.0 g/dL for males and Hb <7.0 g/dL for females.
• Pregnancy or lactation.
• Serum calcium > 10.0 mg/dL or phosphorus > 4.5 mg/dL.
• Subjects with acute kidney injury or rapidly declining GFR.
• Subjects on hemodialysis, peritoneal dialysis, or having a functioning renal transplant.
• Focus of active inflammation such as acute gout, rheumatoid arthritis or active infection determined clinically.