Abstract
Therapy with 1,25(OH)2D3 to prevent osteodystrophy in renal failure patients can cause hypercalcemia, soft tissue calcification, and decreased creatinine clearance. To test whether low dose therapy with 1,25(OH)2D3 could prevent decreased mineralization in uremia without concomitant hypercalcemia, we studied 2 groups (A & B) of 13 rats with remnant kidney and 8 non-remnant controls (C). Groups A & B received 0 μg and .01 μg/Kg/day of 1,25(OH)2D3 respectively. Results: Weekly serum calcium (Ca), phosphorus, creatinine, body weight (wt) were not significantly different between Groups A & B. Analysis after sacrifice at 16 weeks (mean ± 1 SD) showed:
Creatinine correlated inversely with % ash (r=0.77), and femur wt correlated with body wt (r=0.95) in A but not in B. Conclusion: 1,25(OH)2D3 prevented decreased bone mineralization associated with uremia without a significant increase of hypercalcemia, soft tissue calcification, or serum creatinine.
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Sedman, A., Miller, N., Buddington, B. et al. THE EFFECTS OF 1,25(OH)2 D3 ON TISSUE AND BONE METABOLISM IN THE UREMIC RAT MODEL. Pediatr Res 18 (Suppl 4), 369 (1984). https://doi.org/10.1203/00006450-198404001-01659
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DOI: https://doi.org/10.1203/00006450-198404001-01659
