Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-7-1
pubmed:abstractText
Renal bone disease represents one of the major complications of end-stage renal disease, accounting for the numerous and various changes at bone level, determined by abnormal calcium and phosphorus homeostasis and by changes in calcitriol and PTH synthesis. PTH represents as well a major uraemic toxin, exerting profound systemic effects, particularly at the cardiovascular level. PTH synthesis is mainly controlled by changes in calcium-phosphorus balance and calcitriol production by the kidneys. Several others factors are important in the development of secondary hyperparathyroidism: acidosis, autonomisation of PTH secretion and peripheral (target-organ) resistance to PTH actions. Although bone biopsy represents the definitive diagnostic test to differentiate between osteitis fibrosa, low-turnover bone disease and bone involvement unrelated to disturbed calcium metabolism (i.e. beta 2-microglobulin-related amyloidosis), plasma intact PTH generally exhibits a reasonably good relation with bone histology parameters. Moreover serum bone-specific alkaline phosphatase isoenzyme, serum pyridinoline and the novel serum markers for bone turnover are highly specific and correlate with bone histomorphometry parameters, so that, preventive and therapeutic strategies should be re-evaluated based solely on biochemical parameters.
pubmed:language
rum
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0048-7848
pubmed:author
pubmed:issnType
Print
pubmed:volume
104
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
31-5
pubmed:dateRevised
2011-1-13
pubmed:meshHeading
pubmed:articleTitle
[Renal osteodystrophy (I)].
pubmed:affiliation
Facultatea de Medicin?, Universitatea de Medicin? ?i Farmacie Gr.T. Popa Ia?i.
pubmed:publicationType
Journal Article, English Abstract, Review