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ACE Gene Polymorphism and renal responsiveness to ACE inhibitors in IgA nephropathy patients

We examined the renal responsiveness to ACE inhibitor in IgA nephropathy (IgAN) patients according to the grouping of ACE gene polymorphism. Sixty one patients diagnosed as IgAN by renal biopsy and prescribed with ACE inhibitors were enrolled. Genomic DNA was extracted from whole blood and PCR was p...

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Autores principales: Han, Sang Youb, Kwon, Young Joo, Jo, Sang Kyung, Shin, Jin Ho, Cha, Dae Ryong, Cho, Won Yong, Pyo, Heui Jung, Kim, Hyoung Kyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Association of Internal Medicine 2000
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4531733/
https://www.ncbi.nlm.nih.gov/pubmed/10714086
http://dx.doi.org/10.3904/kjim.2000.15.1.13
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author Han, Sang Youb
Kwon, Young Joo
Jo, Sang Kyung
Shin, Jin Ho
Cha, Dae Ryong
Cho, Won Yong
Pyo, Heui Jung
Kim, Hyoung Kyu
author_facet Han, Sang Youb
Kwon, Young Joo
Jo, Sang Kyung
Shin, Jin Ho
Cha, Dae Ryong
Cho, Won Yong
Pyo, Heui Jung
Kim, Hyoung Kyu
author_sort Han, Sang Youb
collection PubMed
description We examined the renal responsiveness to ACE inhibitor in IgA nephropathy (IgAN) patients according to the grouping of ACE gene polymorphism. Sixty one patients diagnosed as IgAN by renal biopsy and prescribed with ACE inhibitors were enrolled. Genomic DNA was extracted from whole blood and PCR was performed. The I/D polymorphism was determined by the presence of the 287 bp fragment in intron 16 of chromosome 17. During the follow-up period (mean; 44.6 months, median: 44.5 months, 5 to 113 months), the blood pressure of 61 patients was controlled below 130/80 mmHg. The renal responsiveness was determined by the degree of changes of proteinuria at 12 months after initiation of ACE inhibitors and by the slope of reciprocal variation of the serum creatinine against follow-up duration {(1/Cr2-1/Cr1)/durations}. The distribution of the II, ID and DD genotype among 61 patients was 21, 16 and 24 patients, respectively. There were no differences among three genotypes in age, sex, the number of patients with initial blood pressure over 140/90 mmHg, initial serum creatinine level, the number of patients with initial azotemia(> 1.4mg/dL) and with initial 24-hr proteinuria amount over 2.0 g. Significant anti-proteinuric effect of ACE inhibitor was found in IgAN(p =0.001), but no significant difference was found among genotypes. Significant difference (p =0.011) was noticed between II type and DD type in the slope of reciprocal variation of the serum creatinine against follow-up duration. In conclusion, efficacy of ACE inhibitors on renal function preservation in IgAN was more pronounced in DD genotype than II genotype.
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spelling pubmed-45317332015-10-02 ACE Gene Polymorphism and renal responsiveness to ACE inhibitors in IgA nephropathy patients Han, Sang Youb Kwon, Young Joo Jo, Sang Kyung Shin, Jin Ho Cha, Dae Ryong Cho, Won Yong Pyo, Heui Jung Kim, Hyoung Kyu Korean J Intern Med Articles We examined the renal responsiveness to ACE inhibitor in IgA nephropathy (IgAN) patients according to the grouping of ACE gene polymorphism. Sixty one patients diagnosed as IgAN by renal biopsy and prescribed with ACE inhibitors were enrolled. Genomic DNA was extracted from whole blood and PCR was performed. The I/D polymorphism was determined by the presence of the 287 bp fragment in intron 16 of chromosome 17. During the follow-up period (mean; 44.6 months, median: 44.5 months, 5 to 113 months), the blood pressure of 61 patients was controlled below 130/80 mmHg. The renal responsiveness was determined by the degree of changes of proteinuria at 12 months after initiation of ACE inhibitors and by the slope of reciprocal variation of the serum creatinine against follow-up duration {(1/Cr2-1/Cr1)/durations}. The distribution of the II, ID and DD genotype among 61 patients was 21, 16 and 24 patients, respectively. There were no differences among three genotypes in age, sex, the number of patients with initial blood pressure over 140/90 mmHg, initial serum creatinine level, the number of patients with initial azotemia(> 1.4mg/dL) and with initial 24-hr proteinuria amount over 2.0 g. Significant anti-proteinuric effect of ACE inhibitor was found in IgAN(p =0.001), but no significant difference was found among genotypes. Significant difference (p =0.011) was noticed between II type and DD type in the slope of reciprocal variation of the serum creatinine against follow-up duration. In conclusion, efficacy of ACE inhibitors on renal function preservation in IgAN was more pronounced in DD genotype than II genotype. Korean Association of Internal Medicine 2000-01 /pmc/articles/PMC4531733/ /pubmed/10714086 http://dx.doi.org/10.3904/kjim.2000.15.1.13 Text en Copyright © 2000 The Korean Association of Internal Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Articles
Han, Sang Youb
Kwon, Young Joo
Jo, Sang Kyung
Shin, Jin Ho
Cha, Dae Ryong
Cho, Won Yong
Pyo, Heui Jung
Kim, Hyoung Kyu
ACE Gene Polymorphism and renal responsiveness to ACE inhibitors in IgA nephropathy patients
title ACE Gene Polymorphism and renal responsiveness to ACE inhibitors in IgA nephropathy patients
title_full ACE Gene Polymorphism and renal responsiveness to ACE inhibitors in IgA nephropathy patients
title_fullStr ACE Gene Polymorphism and renal responsiveness to ACE inhibitors in IgA nephropathy patients
title_full_unstemmed ACE Gene Polymorphism and renal responsiveness to ACE inhibitors in IgA nephropathy patients
title_short ACE Gene Polymorphism and renal responsiveness to ACE inhibitors in IgA nephropathy patients
title_sort ace gene polymorphism and renal responsiveness to ace inhibitors in iga nephropathy patients
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4531733/
https://www.ncbi.nlm.nih.gov/pubmed/10714086
http://dx.doi.org/10.3904/kjim.2000.15.1.13
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