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Received December 29, 2007
Accepted on March 20, 2008
ORIGINAL ARTICLES |
1,
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*Department of Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, and Departments of
Medicine and
Pediatrics, David Geffen School of Medicine at UCLA and
Department of Medicine, Charles Drew University, Los Angeles, California
1 To whom correspondence should be addressed. E-mail: rmehrotra{at}labiomed.org.
| Abstract |
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Background and objectives: Recent studies show high prevalence of suboptimal 25-hydroxyvitamin D levels in chronic kidney disease patients. This study sought to test the hypothesis that the prevalence of 25-hydroxyvitamin D deficiency is significantly higher in chronic kidney disease patients and, in diabetic nephropathy, low serum 25-hydroxyvitamin D is associated with abnormal serum parathyroid hormone, bone mineral density, and coronary artery calcification.
Design, setting, participants, & measurements: Study A used data from the Third National Health and Nutrition Examination Survey. Study B was a post hoc analysis of an observational study of coronary artery calcification in non–dialysis-dependent diabetic nephropathy.
Results: In study A, the adjusted odds for 25-hydroxyvitamin D deficiency were 32% higher in chronic kidney disease patients. This higher prevalence of 25-hydroxyvitamin D deficiency, however, could not be explained by differences in total vitamin D intakes. The consequences of suboptimal 25-hydroxyvitamin D levels were analyzed in 146 patients with diabetic nephropathy. The significant, inverse relationship between serum 25-hydroxyvitamin D and parathyroid hormone levels was attenuated to a nonsignificant level on multivariate adjustment. There was a significant, inverse relationship between bone mineral density and coronary artery calcification scores; neither was independently associated with serum 25-hydroxyvitamin D. The serum 25-hydroxyvitamin D levels declined modestly in 72 patients studied after 12.4 ± 0.4 mo.
Conclusions: 25-Hydroxyvitamin D deficiency is more common in chronic kidney disease, but this higher prevalence is unlikely to be a result of lower vitamin D intakes. The consequences of suboptimal 25-hydroxyvitamin D levels remain to be definitively elucidated.
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T. B. Drueke and E. Ritz Treatment of Secondary Hyperparathyroidism in CKD Patients with Cinacalcet and/or Vitamin D Derivatives Clin. J. Am. Soc. Nephrol., January 1, 2009; 4(1): 234 - 241. [Abstract] [Full Text] [PDF] |
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