FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4234839743> ?p ?o ?g. }

• W4234839743 endingPage "1901" @default.
• W4234839743 startingPage "1899" @default.
• W4234839743 abstract "In their recent contributions to Kidney International, de Zeeuw1.De Zeeuw D. Albuminuria, not only a cardiovascular/renal risk marker, but also a target for treatment?.Kidney Int. 2004; 66: 2-6Google Scholar, as well as de Jong and Brenner2.De Jong P.E. Brenner B.M. From secondary to primary prevention of progressive renal disease: The case for screening for albuminuria.Kidney Int. 2004; 66: 2109-2118Google Scholar, argue that primary prevention of cardiovascular and renal disease may be possible by lowering albumin excretion in subjects with microalbuminuria. Others even advocate screening of the general population for albuminuria as a means to prevent renal and generalized vascular diseases3.Remuzzi G. Weening J.J. Albuminuria as early test for vascular disease.Lancet. 2005; 365: 556-557Google Scholar. We feel that the currently available data do not allow the recommendation of such a policy. It is true that increased levels of albumin excretion are independently associated with the subsequent development of renal insufficiency, as well as with cardiovascular morbidity and mortality. Furthermore, reduction of proteinuria, especially by blockade of the renin-angiotensin system (RAS), has been shown to slow the progression of renal damage in diabetic and nondiabetic renal disease. However, in subjects with microalbuminuria and normal renal function, favorable renal effects of RAS blockade have only been reported for diabetics4.Brenner B.M. Zagrobelny J. Clinical renoprotection trials involving angiotensin II-receptor antagonists and angiotensin-converting-enzyme inhibitors.Kidney Int. 2003; 63: 77-85Google Scholar. Likewise, the only study thus far demonstrating a beneficial effect of reduction of albuminuria on cardiovascular outcome was performed in type 2 diabetics5.De Zeeuw D. Remuzzi G. Parving H.H. et al.Albuminuria, a therapeutic target for cardioavascular protection in type 2 diabetic patients with nephropathy.Circulation. 2004; 110: 921-927Google Scholar. To support the use of albuminuria as a target for primary prevention in a much broader population, the abovementioned authors refer to a recently published study of Asselbergs et al6.Asselbergs F.W. Diercks G.F.H. Hillege H.L. et al.Effects of fosinopril and pravastatin on cardiovascular events in subjects with microalbuminuria.Circulation. 2004; 110: 2809-2816Google Scholar. In this study, subjects with microalbuminuria that were recruited by screening of the general population were randomized to fosinopril or matching placebo and to pravastatin or matching placebo. The results of this study are quoted by de Zeeuw as “Asselbergs et al have indeed shown that ACE inhibitors offer cardiovascular protection in subjects that have no other risk factors than increased amounts of albumin in their urine.” A similar conclusion was drawn by de Jong and Brenner. However, a closer look at the data of Asselbergs et al reveals that this interpretation is not justifiable. First, the effect of fosinopril on the primary cardiovascular end point was not statistically significant, and hard conclusions are, therefore, not allowed. A post-hoc subgroup analysis suggested that especially subjects with an albuminuria level of over 50 mg/24 hr might benefit from treatment with an ACE inhibitor, but this subgroup regarded not even 25% of all individuals. Second, treatment with fosinopril only reduced the incidence of cerebrovascular events, while there was no decrease in any other cardiovascular end point. This disagrees with other prevention studies that consistently show a parallel risk reduction for all types of cardiovascular events7.Yusuf S. Sleight P. Pogue J. et al.Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients: The Heart Outcomes Prevention Evaluation Study Investigators.N Engl J Med. 2000; 342: 145-153Google Scholar, 8.Progress Collaborative Group Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6,105 individuals with previous stroke or transient ischaemic attack.Lancet. 2001; 358: 1033-1041Google Scholar, 9.Heart Protection Study Collaborative Group MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: A randomised placebo-controlled trial.Lancet. 2002; 360: 7-22Google Scholar, 10.Colhoun H.M. Betteridge D.J. Durrington P.N. et al.Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): Multicentre randomised placebo-controlled trial.Lancet. 2004; 364: 685-696Google Scholar. Moreover, treatment with fosinopril did not affect the progression rate of carotid intima-media thickness11.Asselbergs F.W. Van Roon A.M. Hillege H.L. et al.Effects of fosinopril and pravastatin on carotid intima-media thickness in subjects with increased albuminuria.Stroke. 2005; 36: 649-653Google Scholar, while the latter is an accepted surrogate marker for the development of stroke12.Bots M.L. Grobbee D.E. Intima media thickness as a surrogate marker for generalised atherosclerosis.Cardiovasc Drugs Ther. 2002; 16: 341-351Google Scholar. Notably, the incidence of cerebrovascular events in the patients not treated with fosinopril was 6 per 1000 person-years This is very high when compared with reported incidences of 1.5 to 2.1 per 1000 person-years in other low-risk populations13.Solomon S.D. Mcmurray J.J.V. Pfeffer M.A. et al.Cardiovascular risk associated with celecoxib in a clinical trial for colorectal adenoma prevention.N Engl J Med. 2005; 352: 1071-1080Google Scholar , 14.Bresalier R.S. Sandler R.S. Quan H. et al.Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial.N Engl J Med. 2005; 352: 1092-1102Google Scholar, and nearly equals the incidence of stroke observed in type 2 diabetics10.Colhoun H.M. Betteridge D.J. Durrington P.N. et al.Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): Multicentre randomised placebo-controlled trial.Lancet. 2004; 364: 685-696Google Scholar. In fact, the methods section indicates that severe headache for >24 hours without any other abnormality was considered a cerebrovascular accident. In view of all these discrepancies, the type of events that occurred in the control group should be known exactly, to rule out the possibility that ACE inhibition merely reduced the incidence of (severe) headache15.Schrader H. Stovner L.J. Helde G. et al.Prophylactic treatment of migraine with angiotensin converting enzyme inhibitor (lisinopril): randomised, placebo controlled, crossover study.BMJ. 2001; 322: 19-22Google Scholar. Finally, even when considering the effect of ACE inhibition on all end points, the number needed to treat is 38 for four years (i.e., 152 patient-years) to prevent one event, which in our view indicates that it is questionable whether screening and subsequent treatment of microalbuminuria will be cost effective. In conclusion, we think that it is appropriate to regard microalbuminuria as an important risk marker for cardiovascular and renal disease. At present, the value of reducing microalbuminuria has only been proven in diabetic patients. As long as the positive effect of therapy in nondiabetic microalbuminuric patients has not been firmly established, additional studies, including cost-effectiveness analysis, have to be performed before a plea for the implementation of large-scale screening campaigns for microalbuminuria is justified." @default.
• W4234839743 created "2022-05-12" @default.
• W4234839743 creator A5015051666 @default.
• W4234839743 creator A5032487518 @default.
• W4234839743 creator A5055900024 @default.
• W4234839743 date "2005-10-01" @default.
• W4234839743 modified "2023-09-25" @default.
• W4234839743 title "Screening for microalbuminuria" @default.
• W4234839743 doi "https://doi.org/10.1111/j.1523-1755.2005.00578_4.x" @default.
• W4234839743 hasPublicationYear "2005" @default.
• W4234839743 type Work @default.
• W4234839743 citedByCount "0" @default.
• W4234839743 crossrefType "journal-article" @default.
• W4234839743 hasAuthorship W4234839743A5015051666 @default.
• W4234839743 hasAuthorship W4234839743A5032487518 @default.
• W4234839743 hasAuthorship W4234839743A5055900024 @default.
• W4234839743 hasBestOaLocation W42348397431 @default.
• W4234839743 hasConcept C126322002 @default.
• W4234839743 hasConcept C126894567 @default.
• W4234839743 hasConcept C159641895 @default.
• W4234839743 hasConcept C2781203188 @default.
• W4234839743 hasConcept C71924100 @default.
• W4234839743 hasConceptScore W4234839743C126322002 @default.
• W4234839743 hasConceptScore W4234839743C126894567 @default.
• W4234839743 hasConceptScore W4234839743C159641895 @default.
• W4234839743 hasConceptScore W4234839743C2781203188 @default.
• W4234839743 hasConceptScore W4234839743C71924100 @default.
• W4234839743 hasIssue "4" @default.
• W4234839743 hasLocation W42348397431 @default.
• W4234839743 hasOpenAccess W4234839743 @default.
• W4234839743 hasPrimaryLocation W42348397431 @default.
• W4234839743 hasRelatedWork W1999070671 @default.
• W4234839743 hasRelatedWork W2027382735 @default.
• W4234839743 hasRelatedWork W2096516178 @default.
• W4234839743 hasRelatedWork W2119269683 @default.
• W4234839743 hasRelatedWork W2136092602 @default.
• W4234839743 hasRelatedWork W2169713833 @default.
• W4234839743 hasRelatedWork W2416969548 @default.
• W4234839743 hasRelatedWork W2434391732 @default.
• W4234839743 hasRelatedWork W2531580697 @default.
• W4234839743 hasRelatedWork W3145731493 @default.
• W4234839743 hasVolume "68" @default.
• W4234839743 isParatext "false" @default.
• W4234839743 isRetracted "false" @default.
• W4234839743 workType "article" @default.