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THE MOLECULAR-BASIS OF SECONDARY HYPERPARATHYROIDISM IN CHRONIC-RENAL-FAILURE
被引:0
|作者:
RAHAMIMOV, R
SILVER, J
机构:
[1] HADASSAH UNIV HOSP, MINERVA CTR CALCIUM & BONE METAB, NEPHROL SERV, MINERAL METAB UNIT, IL-91120 JERUSALEM, ISRAEL
[2] HEBREW UNIV JERUSALEM, HADASSAH MED SCH, IL-91010 JERUSALEM, ISRAEL
来源:
ISRAEL JOURNAL OF MEDICAL SCIENCES
|
1994年
/
30卷
/
01期
关键词:
PARATHYROID HORMONE;
RENAL FAILURE;
CALCIUM;
PHOSPHATE;
VITAMIN-D;
D O I:
暂无
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
Renal osteodystrophy is a debilitating complication of chronic renal failure and secondary hyperparathyroidism (2HPTH) is one of its central features. 2HPTH develops as a result of the low levels of serum calcium and 1,25-dihydroxyvitamin D [1,25(OH)(2)D-3] the high serum phosphate that occur in chronic renal failure. 1,25(OH)(2)D-3 markedly decreases PTH gene transcription and its lack leads to 2HPTH. A low serum calcium increases PTH mRNA and iPTH levels while a high serum calcium has no effect on PTH gene expression. In experimental uremia there are increased levels of PTH mRNA. In chronic renal failure there is a shift in the calcium set-point to the right. This may be a function of a change in properties of the parathyroid cell calcium receptor, which is a G-protein coupled calcium sensor.
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页码:26 / 31
页数:6
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