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Research Article Free access | 10.1172/JCI106341
Department of Medicine, Columbia University College of Physicians and Surgeons, New York 10032
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215
Gastrointestinal Unit of the Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215
Find articles by Baerg, R. in: JCI | PubMed | Google Scholar
Department of Medicine, Columbia University College of Physicians and Surgeons, New York 10032
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215
Gastrointestinal Unit of the Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215
Find articles by Kimberg, D. in: JCI | PubMed | Google Scholar
Department of Medicine, Columbia University College of Physicians and Surgeons, New York 10032
Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215
Gastrointestinal Unit of the Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215
Find articles by Gershon, E. in: JCI | PubMed | Google Scholar
Published June 1, 1970 - More info
The intestinal absorption of calcium is often depressed in patients with chronic renal insufficiency. Furthermore, the malabsorption of calcium and the osteodystrophy which occur in association with chronic renal disease are often “resistant” to vitamin D; the basis for this resistance remains uncertain however. Recent studies by others have emphasized the role of an abnormality in the metabolism of vitamin D in accounting for the alterations in the calcium absorption and the apparent vitamin D-resistance which accompany the uremic syndrome.
The present studies with an experimentally uremic animal model demonstrate a defect in the active transport of calcium by duodenal gut sacs in vitro. This abnormality is not due to the semistarvation associated with renal insufficiency and cannot be corrected by the administration of physiologic amounts of vitamin D3: it is reversed by massive doses of the vitamin.
Neither the metabolism of vitamin D3 nor the levels of calcium binding protein activity in the duodenal mucosa are affected by renal insufficiency under the conditions employed in the present studies. The results of the present studies strongly suggest that in addition to the recently proposed mechanism involving an interference with the metabolism of vitamin D renal insufficiency also affects the cellular mechanisms for calcium transport in a manner which, while opposite in direction to that of vitamin D, is independent of a direct interaction with the vitamin or its metabolites.