Vitamin D deficiency is associated with a multitude of clinical consequences, including cardiovascular disease (1, 2), decreased bone mineralization (3-5) and early mortality (6). Treatment of 25-hydroxyvitamin D (25-D) deficiency has been associated with positive outcomes including a reduction in falls and improvements in muscle function in elderly individuals (7), reduced risk of hip and nonvertebral fractures (8) and decreased insulin resistance (9). Prospective clinical trials of 25-D supplementation in patients with end-stage renal disease (ESRD) are currently lacking, and the impact of 25-D on clinical outcomes such as bone histomorphology is less clear. Several studies have demonstrated that most hemodialysis (10) and peritoneal dialysis patients are deficient in 25-D (11) and that levels frequently normalize with aggressive supplementation using either ergocalciferol (ERGO) or cholecalciferol (12, 13). The impact of 25-D supplementation on outcomes such as secondary hyperparathyroidism in hemodialysis patients appears to be nominal (14), theoretically because dialysis patients lack the capacity to convert 25-D to 1,25-OH 2 vitamin D (calcitriol), but possibly because the adequate dose for supplementation has yet to be established. While correction of 25-D deficiency appears to have a limited impact on renal osteodystrophy in patients with ESRD, it may improve other clinical outcomes, such as anemia in renal disease. A recent safety and efficacy study of ergocalciferol in hemodialysis patients found a significant reduction in use of recombinant human erythropoietin (EPO) in treated patients (15), with 64% of patients experiencing a reduction in EPO dose after ergocalciferol supplementation. Correction of anemia with EPO has dramatically improved anemia management in hemodialysis patients (16), but

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