Antiproteinuric effect of losartan in non-diabetic renal disease is not dependent on ACE insertion/deletion polymorphism

Hyeong Cheon Park, Hoon Young Choi, Beom Seok Kim, Shin-Wook Kang, Kyu Hun Choi, Sung Kyu Ha, Ho Yung Lee, Dae Suk Han

Research output: Contribution to journalArticle

8 Citations (Scopus)

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 m 2 ) 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.

Original languageEnglish
Pages (from-to)216-224
Number of pages9
JournalKidney and Blood Pressure Research
Volume29
Issue number4
DOIs
Publication statusPublished - 2006 Nov 1

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Losartan
Peptidyl-Dipeptidase A
Proteinuria
Genotype
Kidney
Arterial Pressure
Angiotensin Receptor Antagonists
Chronic Renal Insufficiency
Angiotensin-Converting Enzyme Inhibitors
Creatinine
Blood Pressure

All Science Journal Classification (ASJC) codes

  • Nephrology
  • Cardiology and Cardiovascular Medicine

Cite this

Park, Hyeong Cheon ; Choi, Hoon Young ; Kim, Beom Seok ; Kang, Shin-Wook ; Choi, Kyu Hun ; Ha, Sung Kyu ; Lee, Ho Yung ; Han, Dae Suk. / Antiproteinuric effect of losartan in non-diabetic renal disease is not dependent on ACE insertion/deletion polymorphism. In: Kidney and Blood Pressure Research. 2006 ; Vol. 29, No. 4. pp. 216-224.
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title = "Antiproteinuric effect of losartan in non-diabetic renal disease is not dependent on ACE insertion/deletion polymorphism",
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 m 2 ) 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.",
author = "Park, {Hyeong Cheon} and Choi, {Hoon Young} and Kim, {Beom Seok} and Shin-Wook Kang and Choi, {Kyu Hun} and Ha, {Sung Kyu} and Lee, {Ho Yung} and Han, {Dae Suk}",
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Antiproteinuric effect of losartan in non-diabetic renal disease is not dependent on ACE insertion/deletion polymorphism. / Park, Hyeong Cheon; Choi, Hoon Young; Kim, Beom Seok; Kang, Shin-Wook; Choi, Kyu Hun; Ha, Sung Kyu; Lee, Ho Yung; Han, Dae Suk.

In: Kidney and Blood Pressure Research, Vol. 29, No. 4, 01.11.2006, p. 216-224.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Antiproteinuric effect of losartan in non-diabetic renal disease is not dependent on ACE insertion/deletion polymorphism

AU - Park, Hyeong Cheon

AU - Choi, Hoon Young

AU - Kim, Beom Seok

AU - Kang, Shin-Wook

AU - Choi, Kyu Hun

AU - Ha, Sung Kyu

AU - Lee, Ho Yung

AU - Han, Dae Suk

PY - 2006/11/1

Y1 - 2006/11/1

N2 - 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 m 2 ) 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.

AB - 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 m 2 ) 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.

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