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Genotypes of the renin–angiotensin system and glucocorticoid complications
Author(s) -
Nakamura Akio
Publication year - 2015
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/ped.12434
Subject(s) - medicine , endocrinology , genotype , glucocorticoid , blood pressure , body mass index , single nucleotide polymorphism , prednisolone , plasma renin activity , obesity , snp , renin–angiotensin system , biology , gene , genetics
Background Angiotensinogen ( AGT ) and angiotensin‐converting enzyme ( ACE ) are recognized as important regulators of body mass index ( BMI ) and systemic blood pressure ( BP ). An association between these single nucleotide polymorphisms ( SNP ) of AGT and ACE genes and obesity or hypertension has been established. This study examined relationships between the molecular variants of the AGT and ACE genes and bodyweight or BP in children treated with glucocorticoids for nephrotic syndrome. Methods Twenty J apanese children (male, n = 14; female, n = 6; age, 2–13 years) were genotyped for AGT polymorphisms ( M235T and A‐6G ) and the ACE polymorphisms (insertion/deletion: I / D and rs4341 ). All of the children studied were treated with daily prednisolone 2 mg/kg for 4 weeks and thereafter alternate‐day prednisolone for 8 weeks. BMI , BMI z‐scores, blood lipids, renal function and BP in each group were evaluated during the study period. Results BMI and BMI z‐scores during the glucocorticoid therapy were significantly higher in the TT genotype of the AGT M235T polymorphisms and the AA genotype of the AGT A‐6G polymorphisms compared to other genotypes ( P < 0.05). In contrast, the molecular variant of ACE I /D and rs4341 genotypes did not change bodyweight during the glucocorticoid exposure. It was evident, however, that the BP and blood lipids and renal function were not significantly influenced by the AGT and ACE polymorphisms. Conclusions The TT genotype of the AGT M235T and the AA genotype of the A‐6G polymorphisms may predispose children to bodyweight gain when initially treated with glucocorticoids for nephrotic syndrome.