title: Renin-angiotensin system gene polymorphisms: association with susceptibility to Henoch-Schonlein purpura and renal involvement.
abstract: The clinical course of Henoch-Schönlein Purpura (HSP) in children is variable, with some patients having a much more rapidly progressing course than others. We investigated whether polymorphisms of the renin-angiotensin system (RAS) genes are involved in HSP. Three RAS genotypes were examined in 114 children with HSP and in 164 healthy children: the angiotensin I converting enzyme (ACE) insertion/deletion polymorphism, the M235T mutation in the angiotensinogen gene (Agt), and the A1166C in the angiotensin II type I receptor (AT1R) gene. Significant differences were observed between HSP patients and control group in the frequency of ACE and Agt genotypes (p=0.004 and p=0.003, respectively). The TT genotype of Agt gene was associated with a 3.5-fold increased risk for Henoch-Schönlein nephritis (HSN) compared with the MM/MT genotype (odds ratio, 3.5; 95% confidence interval, 1.2-10.4). There was a trend to a higher prevalence of the TT genotype of the Agt gene among patients with nephrotic range proteinuria when compared to the patients with mild proteinuria, although the difference did not reach a statistical significance. The results of this study suggest that polymorphisms of ACE gene and Agt gene likely influence the risk of developing HSP. However, among the three genes of the RAS studies, only Agt gene was associated with the susceptibility to HSN. RAS gene polymorphisms studied are not associated with the presence of nephrotic range proteinuria. Additional studies are warranted to verify the correlation between RAS gene polymorphisms and susceptibility to HSP.
authors.affiliation: Department of Pediatric Nephrology, Faculty of Medicine, Gazi University, Ankara, Turkey. ozanozkaya@yahoo.com
authors.forename: Ozan
authors.initials: O
authors.lastname: Ozkaya
authors.forename: Oğuz
authors.initials: O
authors.lastname: Söylemezoğlu
authors.forename: Sevim
authors.initials: S
authors.lastname: Gönen
authors.forename: Müge
authors.initials: M
authors.lastname: Misirlioğlu
authors.forename: Serdar
authors.initials: S
authors.lastname: Tuncer
authors.forename: Süleyman
authors.initials: S
authors.lastname: Kalman
authors.forename: Necla
authors.initials: N
authors.lastname: Buyan
authors.forename: Enver
authors.initials: E
authors.lastname: Hasanoğlu
mesh_terms: D000293:Adolescent; D000409:Alanine; D000808:Angiotensinogen / Q000235:genetics; D002648:Child; D002675:Child, Preschool; D003545:Cysteine; D004251:DNA Transposable Elements; D005260:Female; D017353:Gene Deletion; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D011695:IgA Vasculitis / Q000235:genetics*; D007674:Kidney Diseases / Q000235:genetics*; D008297:Male; D008715:Methionine; D009404:Nephrotic Syndrome / Q000652:urine; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D011110:Polymorphism, Genetic; D011507:Proteinuria / Q000235:genetics / Q000503:physiopathology; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics; D012084:Renin-Angiotensin System / Q000235:genetics*; D012720:Severity of Illness Index; D013912:Threonine
chemical_list: D004251:DNA Transposable Elements; D044140:Receptor, Angiotensin, Type 1; D000808:Angiotensinogen; D013912:Threonine; D008715:Methionine; D007703:Peptidyl-Dipeptidase A; D003545:Cysteine; D000409:Alanine