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Antiproteinuric Effect of Losartan in Non-Diabetic Renal Disease Is Not Dependent on ACE Insertion/Deletion Polymorphism

Authors
 Park H.C.  ;  Choi H.Y.  ;  Kim B.S.  ;  Kang S.W.  ;  Choi K.H.  ;  Ha S.K.  ;  Lee H.Y.  ;  Han D.S. 
Citation
 KIDNEY & BLOOD PRESSURE RESEARCH, Vol.29(4) : 216-224, 2006 
Journal Title
 KIDNEY & BLOOD PRESSURE RESEARCH 
ISSN
 1420-4096 
Issue Date
2006
MeSH
Adult ; Angiotensin II Type 1 Receptor Blockers/administration & dosage* ; Blood Pressure/drug effects ; Diuretics/administration & dosage ; Drug Therapy, Combination ; Female ; Gene Deletion ; Genotype ; Humans ; Losartan/administration & dosage* ; Male ; Middle Aged ; Peptidyl-Dipeptidase A/genetics* ; Polymorphism, Genetic ; Prevalence ; Proteinuria/drug therapy* ; Proteinuria/epidemiology ; Proteinuria/genetics* ; Treatment Outcome
Keywords
Angiotensin-converting enzyme gene polymorphism ; Losartan Nephropathy, non-diabetic ; Proteinuria
Abstract
Background: The antiproteinuric effect of angiotensin-converting enzyme (ACE) inhibitors appears to vary depending on the ACE insertion (I)/deletion (D) genotype in non-diabetic nephropathy. This interaction may be overcome by using an angiotensin II receptor blocker. We evaluated the short-term antiproteinuric effect of losartan according to the ACE I/D genotype in patients with non-diabetic proteinuric renal diseases. Methods: Ninety-nine (II/ID/DD: 36/52/11) non-diabetic patients with overt proteinuria were enrolled. The patients received losartan 50 mg daily followed by 100 mg in two treatment periods each lasting 12 weeks. Clinical parameters including proteinuria were measured at baseline and at the end of each period. Results: At baseline each genotype (II/ID/DD) had comparable mean arterial blood pressure (mean ± SD) 103.2 ± 11.1/102.7 ± 10.6/104.1 ± 15.3; proteinuria (geometric mean, 95% CI, mg/day) 1,839 (1,518–2,227)/1,998 (1,683–2,372)/1,613 (1,072–2,427), and creatinine clearance (ml/min/1.73 m2) 65.7 ± 28.4/63.2 ± 27.8/68.8 ± 25.3, respectively. Both doses of losartan significantly lowered blood pressure and proteinuria (p < 0.05 vs. baseline), and losartan 100 mg was more effective than 50 mg in reducing proteinuria (52.5 ± 29.0 vs. 40.5 ± 30.8%, respectively, p = 0.001). No differences in the antiproteinuric effect of losartan was observed among the ACE I/D genotype. Losartan 100 mg demonstrated a comparable degree of mean arterial pressure (mean ± SD, %) (II/ID/DD, 13.3 ± 7.6/10.8 ± 9.8/13.0 ± 11.6, respectively, p = NS) and proteinuria reduction (mean, 95% CI) among the three genotypes (51.4% (40.3–62.5%)/53.4% (45.5–61.4%)/51.4% (40.0–63.8%), respectively, p = NS). Conclusion: Our data suggest that losartan provides a similar short-term antiproteinuric response for all three genotypes of ACE I/D genotype in non-diabetic proteinuric chronic renal disease.
Full Text
http://www.karger.com/Article/Fulltext/95736
DOI
10.1159/000095736
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kang, Shin Wook(강신욱) ORCID logo https://orcid.org/0000-0002-5677-4756
Kim, Beom Seok(김범석) ORCID logo https://orcid.org/0000-0002-5732-2583
Park, Hyeong Cheon(박형천) ORCID logo https://orcid.org/0000-0002-1550-0812
Choi, Kyu Hun(최규헌) ORCID logo https://orcid.org/0000-0003-0095-9011
Choi, Hoon Young(최훈영) ORCID logo https://orcid.org/0000-0002-4245-0339
Ha, Sung Kyu(하성규)
Han, Dae Suk(한대석)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/109047
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