Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1996-12-3
pubmed:abstractText
Recent clinical and experimental data suggest that the resistance of parathyroid cells to the physiological concentration of calcitriol plays an important role in the pathogenesis and the progression of secondary hyperparathyroidism in chronic renal failure. This resistance is due to the decreased density of the calcitriol receptor in parathyroid cells, which may result from impaired upregulation of calcitriol receptor. Since patients with larger parathyroid glands were more resistance to calcitriol pulse therapy than those with smaller glands and calcitriol receptor density inversely correlated with gland weight, the size of the parathyroid gland may serve as a marker for the degree of resistance to calcitriol. Furthermore, the possible role of phosphorus in the control of parathyroid function has been suggested recently. Thus, it is most important to prevent the progression of parathyroid hyperplasia in chronic renal failure by the early use of active vitamin D, calcitriol pulse therapy, and dietary phosphorus restriction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0160-564X
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1210-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Molecular basis for the management of secondary hyperparathyroidism in chronic renal failure.
pubmed:affiliation
First Department of Internal Medicine, University of Tokyo, Japan.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't