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Renin-angiotensin system gene polymorphisms in children with Henoch-Schonlein purpura in West China.

Authors: Desong, LIU  Fang, LU  Songhui, ZHAI  Liu, WEI  Shi, MA  Xiuying, CHEN  Liqun, DONG  Yannan, GUO  Jin, WU  Zheng, WANG 
Citation: Desong Liu, etal., J Renin Angiotensin Aldosterone Syst. 2010 Dec;11(4):248-55. doi: 10.1177/1470320310374214. Epub 2010 Aug 11.
Pubmed: (View Article at PubMed) PMID:20702504
DOI: Full-text: DOI:10.1177/1470320310374214

It has been suggested that renin-angiotensin system (RAS) gene polymorphism is involved in the pathogenesis of Henoch-Schonlein purpura (HSP) with conflicting reports. We therefore investigate the effect of RAS gene polymorphism on HSP susceptibility and severity in a Chinese cohort. The study included 142 children with HSP and 218 healthy controls that were genotyped for RAS gene polymorphisms. Significantly, differences of T174M-T and ACE-D frequency were found between HSP patients and controls (p(alleo) = .002, OR(alleo) = 2.001; p(alleo) = .007, OR(alleo) = 1.533, respectively). We also found correlations between ACE-I/D and Agt T174M with multiple organ involvements, with significant differences in ACE-D in renal groups (p < 0.05) and Agt T174M in non-renal (p(joint) = .002, p(GI) = .042). Furthermore, decreasing M235T-T and increasing ACE-D were found associated with serious renal complications (p = .019, p = .016). Additionally, ACE-I/D and T174M were significantly associated with high clinical score patients, as opposed to low clinical score patients, when patients were scored depending on the severity of overall complications (p = .045, p = .026). We suggest that RAS gene polymorphisms (ACE-I/D, M235T or T174M) are significantly associated with susceptibility to HSP, organ involvement, and disease severity, which largely account for individual prognosis.

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CRRD Object Information
CRRD ID: 11039055
Created: 2016-03-01
Species: All species
Last Modified: 2016-03-01
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.