Abstract
INTESTINAL malabsorption of calcium occurs regularly in patients with advanced renal failure and is commonly associated with rickets or osteomalacia, which closely resemble the osteodystrophy of vitamin D deficiency1. Large amounts of vitamin D are required to correct this defect in calcium absorption and to promote healing of the bone lesions but the nature of the relative insensitivity to the biological effects of the vitamin is uncertain1,2. The suggestion3 that vitamin D resistance in uraemia is due to an effective deficiency of 25-hydroxycholecalciferol has been refuted2,4. The demonstration of the role of the kidney in producing a second biologically potent metabolite, 1,25-dihydroxycholecalciferol5,6, makes it likely that the abnormalities in uraemic patients are due to loss of renal tissue (see preceding communication7).
Published Version
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