Linked Life Data

17721071

Source:http://linkedlifedata.com/resource/pubmed/id/17721071

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6 Suppl
pubmed:dateCreated
2007-8-27
pubmed:abstractText
Hyperphosphatemia indicates a plasma inorganic phosphate (Pi) concentration greater than 5 mg/dl in the adult and 7 mg/dl in adolescent subjects. Pi homeostasis is maintained by several mechanisms (intestinal absorption, renal excretion, balance of Pi exchanges in and out of the cells, hormonal regulation). Most of the Pi, after intestinal absorption, undergoes urinary excretion suggesting that the kidney plays a major role in the maintenance of homeostasis and plasma concentration of the Pi, modifying its reabsorption in the proximal tubule where 3 types of sodium/ phosphate cotransporters have been identified (NPT). NPT2 is crucial for the Pi reabsorption and is modulated by several hormones (PTH and vitamin D3, phosphatonins) and non-hormonal factors. The hyperphospatemia is usually due to a decrease in renal function or a PTH absence (primary or secondary hypoparathyroidism) or phosphatonin deficiency. A correct serum Pi concentration is a critical condition for maintaining the calcium-phosphate (CaxPi) product within a safe range ensuring the physiological processes of bone mineralization; an increase of CaxPi product in extracellular fluids over a critical threshold, may promote processes of extraskeletal calcification. In the last few years several studies have shown that the pathogenetic mechanisms of vascular calcification do not imply a simple deposition of calcium phosphate crystals in the wall of the vessels affected by atherosclerotic lesions, but an active process making vascular smooth cells assume functional characteristics of osteoblasts. The consequences on bone are heterogeneous according to the pathogenetic mechanisms responsible for hyperphosphatemia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1720-8386
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
29-34
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Hyperphosphatemia: effects on bone metabolism and cardiovascular risk.
pubmed:affiliation
Department of Clinical Medicine and Applied Biotechnology D. Campanacci, University of Bologna, Bologna, Italy. renata.caudarella@alice.it
pubmed:publicationType
Journal Article, Review