Linked Life Data

16336578

Source:http://linkedlifedata.com/resource/pubmed/id/16336578

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
99
pubmed:dateCreated
2005-12-12
pubmed:abstractText
The renin-angiotensin-aldosterone system (RAAS) is a well known regulator of blood pressure (BP) and determinant of target-organ damage. It controls fluid and electrolyte balance through coordinated effects on the heart, blood vessels, and Kidneys. Angiotensin II (AII) is the main effector of the RAAS and exerts its vasoconstrictor effect predominantly on the postglomerular arterioles, thereby increasing the glomerular hydraulic pressure and the ultrafiltration of plasma proteins, effects that may contribute to the onset and progression of chronic renal damage. AII may also directly contribute to accelerate renal damage by sustaining cell growth, inflammation, and fibrosis. Interventions that inhibit the activity of the RAAS are renoprotective and may slow or even halt the progression of chronic nephropathies. ACE inhibitors and angiotensin II receptor antagonists can be used in combination to maximize RAAS inhibition and more effectively reduce proteinuria and GFR decline in diabetic and nondiabetic renal disease. Recent evidence suggests that add-on therapy with an aldosterone antagonist may further increase renoprotection, but may also enhance the risk hyperkalemia. Maximized RAAS inhibition, combined with intensified blood pressure control (and metabolic control in diabetics) and amelioration of dyslipidemia in a multimodal approach including lifestyle modifications (Remission Clinic), may achieve remission of proteinuria and renal function stabilization in a substantial proportion of patients with proteinuric renal disease. Ongoing studies will tell whether novel drugs inhibiting the RAAS, such as the renin inhibitors or the vasopeptidase inhibitors, may offer additional benefits to those who do not respond, or only partially respond, to this multimodal regimen.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0098-6577
pubmed:author
pubmed:issnType
Print
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S57-65
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16336578-Angiotensin II Type 1 Receptor Blockers, pubmed-meshheading:16336578-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:16336578-Animals, pubmed-meshheading:16336578-Blood Pressure, pubmed-meshheading:16336578-Chronic Disease, pubmed-meshheading:16336578-Disease Progression, pubmed-meshheading:16336578-Drug Therapy, Combination, pubmed-meshheading:16336578-Glomerular Filtration Rate, pubmed-meshheading:16336578-Humans, pubmed-meshheading:16336578-Kidney Diseases, pubmed-meshheading:16336578-Kidney Failure, Chronic, pubmed-meshheading:16336578-Nephritis, pubmed-meshheading:16336578-Polymorphism, Genetic, pubmed-meshheading:16336578-Receptors, Aldosterone, pubmed-meshheading:16336578-Renin, pubmed-meshheading:16336578-Renin-Angiotensin System, pubmed-meshheading:16336578-Transplantation Tolerance
pubmed:year
2005
pubmed:articleTitle
The role of renin-angiotensin-aldosterone system in the progression of chronic kidney disease.
pubmed:affiliation
Unit of Nephrology, Azienda Ospedaliera Ospedali Riuniti di Bergamo, Italy. gremuzzi@marionegri.it
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't