Details
| Originalsprache | Englisch |
|---|---|
| Seiten (von - bis) | 606-615 |
| Seitenumfang | 10 |
| Fachzeitschrift | Clinical Transplantation |
| Jahrgang | 23 |
| Ausgabenummer | 5 |
| Publikationsstatus | Veröffentlicht - Sept. 2009 |
| Extern publiziert | Ja |
Abstract
Renin-angiotensin-aldosterone system (RAAS) polymorphisms such as the angiotensinogen-gene-M235T-, the angiotensin-conversion enzyme (ACE)-gene I/D- and the angiotensin-II-type 1-receptor-(AT1R)-A1166C-polymorphism have been implicated in renal insufficiency and hypertension. We studied the association of these RAAS genotypes and non-genetic factors with transplant function and hypertension after renal graft transplantation (NTX). A total of 229 renal graft recipients, transplanted at a single center, were monitored up to 54 months and genotyped using polymerase chain reaction. The prevalence of the genotypes was comparable to a control group of healthy volunteers. Genotype and clinical outcome was analyzed using anova, while the k-nearest neighbor method was used for a pattern recognition analysis of the complete database. Hypertension after NTX was not influenced by the RAAS polymorphisms. The DD-genotype of the ACE-I/D-polymorphism was associated with significantly deteriorated renal transplant function during the months 18 to 30 after transplantation according to anova at p < 0.05, as were non-genetic factors like long hospitalization, poor primary transplant function, and frequent rejections. Pattern recognition identified, the use of cyclosporine (odds ratio of 4.25) and the use of Ang II-receptor-blockers at discharge indicating the need of effective antihypertensive treatment (odds ratio of 3.26) as risk factors for transplant function loss. Altogether, the significant impact of the DD-genotype on the outcome after renal transplantation emphasizes the early identification of RAAS genotypes.
ASJC Scopus Sachgebiete
- Medizin (insg.)
- Transplantationsmedizin
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in: Clinical Transplantation, Jahrgang 23, Nr. 5, 09.2009, S. 606-615.
Publikation: Beitrag in Fachzeitschrift › Artikel › Forschung › Peer-Review
}
TY - JOUR
T1 - Impact of genetic polymorphisms of the renin-angiotensin system and of non-genetic factors on kidney transplant function
T2 - A single-center experience
AU - Siekierka-Harreis, Magdalena
AU - Kuhr, Nicola
AU - Willers, Rainhart
AU - Ivens, Katrin
AU - Grabensee, B.
AU - Mondry, Adrian
AU - Loh, Marie C.S.
AU - Rump, Lars Christian
AU - Blume, Cornelia
PY - 2009/9
Y1 - 2009/9
N2 - Renin-angiotensin-aldosterone system (RAAS) polymorphisms such as the angiotensinogen-gene-M235T-, the angiotensin-conversion enzyme (ACE)-gene I/D- and the angiotensin-II-type 1-receptor-(AT1R)-A1166C-polymorphism have been implicated in renal insufficiency and hypertension. We studied the association of these RAAS genotypes and non-genetic factors with transplant function and hypertension after renal graft transplantation (NTX). A total of 229 renal graft recipients, transplanted at a single center, were monitored up to 54 months and genotyped using polymerase chain reaction. The prevalence of the genotypes was comparable to a control group of healthy volunteers. Genotype and clinical outcome was analyzed using anova, while the k-nearest neighbor method was used for a pattern recognition analysis of the complete database. Hypertension after NTX was not influenced by the RAAS polymorphisms. The DD-genotype of the ACE-I/D-polymorphism was associated with significantly deteriorated renal transplant function during the months 18 to 30 after transplantation according to anova at p < 0.05, as were non-genetic factors like long hospitalization, poor primary transplant function, and frequent rejections. Pattern recognition identified, the use of cyclosporine (odds ratio of 4.25) and the use of Ang II-receptor-blockers at discharge indicating the need of effective antihypertensive treatment (odds ratio of 3.26) as risk factors for transplant function loss. Altogether, the significant impact of the DD-genotype on the outcome after renal transplantation emphasizes the early identification of RAAS genotypes.
AB - Renin-angiotensin-aldosterone system (RAAS) polymorphisms such as the angiotensinogen-gene-M235T-, the angiotensin-conversion enzyme (ACE)-gene I/D- and the angiotensin-II-type 1-receptor-(AT1R)-A1166C-polymorphism have been implicated in renal insufficiency and hypertension. We studied the association of these RAAS genotypes and non-genetic factors with transplant function and hypertension after renal graft transplantation (NTX). A total of 229 renal graft recipients, transplanted at a single center, were monitored up to 54 months and genotyped using polymerase chain reaction. The prevalence of the genotypes was comparable to a control group of healthy volunteers. Genotype and clinical outcome was analyzed using anova, while the k-nearest neighbor method was used for a pattern recognition analysis of the complete database. Hypertension after NTX was not influenced by the RAAS polymorphisms. The DD-genotype of the ACE-I/D-polymorphism was associated with significantly deteriorated renal transplant function during the months 18 to 30 after transplantation according to anova at p < 0.05, as were non-genetic factors like long hospitalization, poor primary transplant function, and frequent rejections. Pattern recognition identified, the use of cyclosporine (odds ratio of 4.25) and the use of Ang II-receptor-blockers at discharge indicating the need of effective antihypertensive treatment (odds ratio of 3.26) as risk factors for transplant function loss. Altogether, the significant impact of the DD-genotype on the outcome after renal transplantation emphasizes the early identification of RAAS genotypes.
KW - Angiotensin II-type receptor gene A1166C polymorphism
KW - Angiotensin-converting enzyme gene I/D polymorphism
KW - Angiotensinogen gene M235T polymorphism
KW - Clinical study
KW - K-nearest neighbor
KW - Pattern recognition
KW - Risk factors
KW - Transplant function loss
UR - http://www.scopus.com/inward/record.url?scp=70350158809&partnerID=8YFLogxK
U2 - 10.1111/j.1399-0012.2009.01033.x
DO - 10.1111/j.1399-0012.2009.01033.x
M3 - Article
C2 - 19681973
AN - SCOPUS:70350158809
VL - 23
SP - 606
EP - 615
JO - Clinical Transplantation
JF - Clinical Transplantation
SN - 0902-0063
IS - 5
ER -