Determinants of Intact Parathyroid Hormone and Free 1,25-Dihydroxyvitamin D Levels in Mild and Moderate Renal Failure
作者:
Andrew St. John,
Mark B. Thomas,
Charmian P. Davies,
Brian Mullan,
Ian Dick,
Brian Hutchison,
Agatha van der Schaff,
Richard L. Prince,
期刊:
Nephron
(Karger Available online 1992)
卷期:
Volume 61,
issue 4
页码: 422-427
ISSN:1660-8151
年代: 1992
DOI:10.1159/000186960
出版商: S. Karger AG
关键词: Chronic renal failure;Intact PTH;1;25-Dihydroxyvitamin D
数据来源: Karger
摘要:
Parameters of calcium and phosphate metabolism were measured in 27 patients with mild renal failure [glomerular filtration rate (GFR) 40-90 ml/min], 12 patients with moderate renal failure (GFR 20-39 ml/min) and in 12 healthy subjects. GFR was determined by technetium-99m diethylenetriamine pentaacetic acid clearance. Intact parathyroid hormone (PTH) was measured by a sensitive immunochemiluminometric assay and somatomedin-C was determined by radioimmunoassay. Both 1,25-dihydroxyvitamin D [1,25(OH)2D] and vitamin-D-binding protein were measured allowing calculation of the free 1,25(OH)2D index. By linear regression and multivariate analysis, PTH was negatively and independently correlated with GFR, plasma bicarbonate and 25-hydroxyvitamin D [25(OH)D] while free 1,25(OH)2D was positively correlated with GFR. Increased PTH secretion and reductions in 1,25(OH)2D were present in mild renal failure patients before any changes in plasma calcium, phosphate and bicarbonate were noted. Plasma alkaline phosphatase was significantly higher in mild chronic renal failure patients compared to normal subjects, possibly indicating early effects of the secondary hyperparathyroidism on the skeleton. Somatomedin-C did not correlate with the free 1,25(OH)2D index or a measure of 1,25(OH)2D production. It is concluded that the secondary hyperparathyroidism which occurs very early in the onset of chronic renal failure may be due to a reduction in the circulating concentration of 1,25(OH)2D consequent upon the renal failure. Low plasma bicarbonate and 25(OH)D also appear to be determinants of a raised PTH concentration. The compensatory increase in PTH presumably maintains extracellular calcium and phosphate levels constant but with possible deleterious effects on the skeleton.
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