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Article: Angiotensin converting enzyme inhibition for cardiac hypertrophy in patients with end-stage renal disease: What is the evidence?

TitleAngiotensin converting enzyme inhibition for cardiac hypertrophy in patients with end-stage renal disease: What is the evidence?
Authors
KeywordsAngiotensin II
Issue Date2004
Citation
Nephrology, 2004, v. 9, n. 4, p. 190-197 How to Cite?
AbstractDialysis patients show a high prevalence of cardiovascular complications among which left ventricular hypertrophy is one of the most frequent and is independently predictive of mortality. A recent study indicates that partial regression of left ventricular hypertrophy improves mortality and reduces cardiovascular events in end-stage renal disease (ESRD) patients, suggesting the importance of targeting therapeutic strategies to reduce cardiac hypertrophy and improve the outcome in these patients. The pathogenesis of left ventricular hypertrophy in ESRD patients is multifactorial and includes hypertension, activation of the renin-angiotensin system, increased sympathetic activity, chronic volume overload, chronic anaemia and hyperparathyroidism. In this paper, we review the available experimental and clinical evidence showing the important contribution of the renin-angiotensin system as well as its interaction with the sympathetic nervous system in the pathogenesis of left ventricular hypertrophy in ESRD patients. Furthermore, we summarize the results of currently available clinical studies that examined the effects of angiotensin-converting enzyme inhibition or angiotensin receptor antagonism on left ventricular hypertrophy in ESRD patients, and review evidences that support the use of angiotensin-converting enzyme inhibitors or angiotensin receptor antagonists in the ESRD population.
Persistent Identifierhttp://hdl.handle.net/10722/228456
ISSN
2015 Impact Factor: 1.796
2015 SCImago Journal Rankings: 0.894

 

DC FieldValueLanguage
dc.contributor.authorWang, Angela Yee Moon-
dc.contributor.authorLi, Philip Kam Tao-
dc.contributor.authorLui, Siu Fai-
dc.contributor.authorSanderson, John E.-
dc.date.accessioned2016-08-13T08:02:27Z-
dc.date.available2016-08-13T08:02:27Z-
dc.date.issued2004-
dc.identifier.citationNephrology, 2004, v. 9, n. 4, p. 190-197-
dc.identifier.issn1320-5358-
dc.identifier.urihttp://hdl.handle.net/10722/228456-
dc.description.abstractDialysis patients show a high prevalence of cardiovascular complications among which left ventricular hypertrophy is one of the most frequent and is independently predictive of mortality. A recent study indicates that partial regression of left ventricular hypertrophy improves mortality and reduces cardiovascular events in end-stage renal disease (ESRD) patients, suggesting the importance of targeting therapeutic strategies to reduce cardiac hypertrophy and improve the outcome in these patients. The pathogenesis of left ventricular hypertrophy in ESRD patients is multifactorial and includes hypertension, activation of the renin-angiotensin system, increased sympathetic activity, chronic volume overload, chronic anaemia and hyperparathyroidism. In this paper, we review the available experimental and clinical evidence showing the important contribution of the renin-angiotensin system as well as its interaction with the sympathetic nervous system in the pathogenesis of left ventricular hypertrophy in ESRD patients. Furthermore, we summarize the results of currently available clinical studies that examined the effects of angiotensin-converting enzyme inhibition or angiotensin receptor antagonism on left ventricular hypertrophy in ESRD patients, and review evidences that support the use of angiotensin-converting enzyme inhibitors or angiotensin receptor antagonists in the ESRD population.-
dc.languageeng-
dc.relation.ispartofNephrology-
dc.subjectAngiotensin II-
dc.titleAngiotensin converting enzyme inhibition for cardiac hypertrophy in patients with end-stage renal disease: What is the evidence?-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1440-1797.2004.00260.x-
dc.identifier.pmid15363049-
dc.identifier.scopuseid_2-s2.0-4844220824-
dc.identifier.volume9-
dc.identifier.issue4-
dc.identifier.spage190-
dc.identifier.epage197-

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