INFLUENCE OF METABOLIC-ACIDOSIS ON SERUM 1,25(OH)2D3 LEVELS IN CHRONIC-RENAL-FAILURE

Citation
Kc. Lu et al., INFLUENCE OF METABOLIC-ACIDOSIS ON SERUM 1,25(OH)2D3 LEVELS IN CHRONIC-RENAL-FAILURE, Mineral and electrolyte metabolism, 21(6), 1995, pp. 398-402
Citations number
25
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
03780392
Volume
21
Issue
6
Year of publication
1995
Pages
398 - 402
Database
ISI
SICI code
0378-0392(1995)21:6<398:IOMOS1>2.0.ZU;2-8
Abstract
Metabolic acidosis has been shown to alter vitamin D metabolism. There is also evidence that calcium may modulate 1,25(OH)(2)D-3 by a parath yroid hormone (PTH)-independent mechanism. To investigate the effect o f rapid correction of chronic metabolic acidosis on serum 1,25(OH)(2)D -3 levels by free calcium clamp in chronic renal failure, 20 patients with mild to moderate metabolic acidosis (mean pH 7.31 +/- 0.04) and s econdary hyperparathyroidism (mean intact PTH 156.47 +/- 84.20 ng/l) w ere enrolled in this study. None had yet received any dialysis therapy . Metabolic acidosis was corrected by continuous bicarbonate infusion for 3-4 h until plasma pH was around 7.4, while plasma ionized calcium was held at the preinfusion level by calcium solution infusion during the entire procedure. The plasma pH, bicarbonate, total CO2, sodium, and serum total calcium levels were significantly increased while seru m concentrations of alkaline phosphatase and albumin were significantl y decreased after bicarbonate infusion. The plasma ionized calcium, po tassium, serum magnesium, inorganic phosphorus, and 25(OH)D levels sho wed no significant change before and after bicarbonate infusion. The s erum 1,25(OH)(2)D-3 levels were significantly increased (38.66 +/- 11. 77 vs. 47.04 +/- 16.56 pmol/l, p < 0.05) after correction of metabolic acidosis. These results demonstrate that rapid correction of metaboli c acidosis raises serum 1,25(OH)(2)D-3 levels in vitamin D-deficient c hronic renal failure patients, and may underline the importance of mai ntaining normal acid-base homeostasis in the presence of secondary hyp erparathyroidism in chronic renal failure.