Effect of daily oral vitamin D and calcium therapy, hypophosphatemia, and endogenous 1-25 dihydroxycholecalciferol on parathyroid hormone and phosphate wasting in renal transplant recipients.
Ten stable, normocalcemic renal transplant patients with good allograft function, hyperparathyroidism, and variable hypophosphatemia were treated for 2 to 9 months with oral calcium carbonate and replacement doses of vitamin D analogues. Parathyroid hormone levels (PTH) and renal phosphate wasting were not autonomous or fixed but decreased with therapy. Although serum 1-25(OH)2D3 levels could be shown to rise appropriately during oral vitamin D therapy and fall afterwards, a separate study in a larger group of patients showed no effect of elevated parathyroid hormone or hypophosphatemia to increase endogenous 1-25(OH)2D3 levels. Some 42% of patients with elevated carboxy-terminal PTH, had elevated N-terminal PTH, which was closely associated with more severe phosphate wasting. Aggressive oral calcium and vitamin D supplementation in certain normocalcemic renal transplant patients may decrease endogenous PTH levels, improve hypophosphatemia, and provide a physiologic increase in levels of 1-25(OH)2D3.
Steiner
R W
RW
Department of Medicine, UCSD Medical Center 92103-8781.
Ziegler
M
M
Halasz
N A
NA
Catherwood
B D
BD
Manolagas
S
S
Deftos
L J
LJ
D000284:Administration, Oral; D002117:Calcitriol / Q000097:blood*; D002119:Calcium Carbonate / Q000008:administration & dosage / Q000627:therapeutic use*; D003404:Creatinine / Q000097:blood; D004097:Dihydrotachysterol / Q000627:therapeutic use; D005500:Follow-Up Studies; D006801:Humans; D016030:Kidney Transplantation / Q000502:physiology*; D010281:Parathyroid Hormone / Q000097:blood*; D010710:Phosphates / Q000097:blood*; D013997:Time Factors; D014807:Vitamin D / Q000008:administration & dosage / Q000627:therapeutic use*
D010281:Parathyroid Hormone; D010710:Phosphates; D014807:Vitamin D; D003404:Creatinine; D002117:Calcitriol; D002119:Calcium Carbonate; D004097:Dihydrotachysterol