Abstract
Chronic renal disease is characteristically attended by derangements in calcium homeostasis and bone metabolism. 1-3 Many investigators have documented an impaired intestinal absorption of calcium in patients with chronic renal failure using either classical metabolic balance or isotopic marking techniques. 3-5 This defect has also been noted in patients without manifest azotemia or acidosis 3,6 and has been confirmed in chronic experimental renal insufficiency by Kessner and Epstein. 7 Liu and Chu initially considered a "resistance" to vitamin D action in the uremic individual as a cause for defective intestinal calcium absorption. 8 Stanbury and Lumb 3 and Dent and co-workers 9 have also suggested that the "acquired vitamin D resistance" results primarily in the defective absorption of calcium from the gastrointestinal tract. The subsequent studies of Fletcher et al made during the therapeutic trials of alkali, aluminum hydroxide, vitamin D, and calcium supplements in uremic osteodystrophic patients appear confirmatory
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