Linked Life Data

18550649

Source:http://linkedlifedata.com/resource/pubmed/id/18550649

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2008-7-29
pubmed:abstractText
The renin-angiotensin-aldosterone system (RAS) is a widely known regulator of BP and a determinant of target organ damage. Angiotensin II, the main effector of RAS, is a key mediator of renal injury by increasing intraglomerular capillary pressure and ultrafiltration of plasma proteins and by promoting cell growth and fibroproliferative effects. RAS blockade with inhibitors of RAS is beneficial in slowing progressive loss of renal function in chronic kidney disease. Experimental evidence also indicates that aldosterone, besides being a regulator of extracellular fluid volume and sodium and potassium balance, directly contributes to accelerate renal damage by sustaining cell growth, inflammation, and fibrosis. This occurs through production of growth factors and reactive oxygen species as well as inhibition of extracellular matrix degradation. Attenuation of growth-promoting and fibroproliferative effect of aldosterone may contribute to protection against progressive renal injury. Initial studies that detail the efficacy of aldosterone blockade in animals and humans are encouraging. Nevertheless, further studies in larger populations with longer follow-up are warranted to address more definitely the safety and renoprotective effect of aldosterone antagonism in chronic kidney disease patients.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1533-3450
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1459-62
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
The aggravating mechanisms of aldosterone on kidney fibrosis.
pubmed:affiliation
Department of Medicine and Transplantation, Ospedali Riuniti di Bergamo, Mario Negri Institute for Pharmacological Research, Bergamo, Italy. gremuzzi@marionegri.it
pubmed:publicationType
Journal Article