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ADC Fetal and Neonatal Edition Letters and ADC Education and Practice Letters
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Jae Seung Lee, Pediatric Nephrologist, Professor Department of Paediatrics, Yonsei University College of Medicine, Seoul, Korea, Jae Il Shin, and Jae Seung Lee
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jsyonse{at}yumc.yonsei.ac.kr Jae Seung Lee, et al.
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Dear Editor, Recently, the studies on polymorphism of the angiotensin-converting enzyme (ACE) gene in patients with Henoch-Schonlein purpura (HSP) have been performed in different countries. Yoshioka et al. reported that the incidence of moderate to heavy proteinuria was significantly higher in HSP nephritis patients with the DD genotype than in the II or ID genotype.[1] However, subsequent analyses did not show this trend of the ACE gene polymorphism in patients with HSP nephritis.[2-4] Also, Ha et al. demonstrated that there was no difference in the ACE genotype between 33 children with HSP (DD: 25%, ID: 50%, II: 25%) and 28 with HSP nephritis (DD: 24%, ID: 46%, II: 30%).[5] Recently, Zhou et al. investigated the polymorphism of ACE gene in 103 patients with HSP nephritis and 100 healthy children. In this study, DD genotype was more frequently seen in children with HSP nephritis than in normal children, and associated with gross haematuria, massive proteinuria and severe pathologic classes in patients with HSP nephritis.[6] However, Choi et al. demonstrated that polymorphism of the ACE gene did not differ between 75 patients with HSP nephritis (DD: 12%, ID: 51%, II: 37%) and 100 healthy control subjects (DD: 17%, ID: 49%, II: 34%) and was not related to the clinical outcome at the last follow-up in children with HSP nephritis (favourable outcome; DD: 9 (15%), ID: 28 (46%), II: 24 (39%) vs unfavourable outcome; DD: 0 (0%), ID: 10 (71%), II: 4 (29%)).[7] Therefore, it would be difficult to evaluate the susceptibility of HSP or nephritis and prognosis in an individual patient by polymorphism of the ACE gene due to these controversial results and further studies in a large cohort are necessary to elucidate the role of renin angiotensin system in the pathogenesis of HSP or HSP nephritis. References 1. Yoshioka T, Xu YX, Yoshida H, Shiraga H, Muraki T, Ito K. Deletion polymorphism of the angiotensin converting enzyme gene predicts persistent proteinuria in Henoch-Schonlein purpura nephritis. Arch Dis Child 1998;79:394-399. 2. Amoroso A, Danek G, Vatta S, et al. Polymorphisms in angiotensin- converting enzyme gene and severity of renal disease in Henoch-Schoenlein patients. Italian Group of Renal Immunopathology. Nephrol Dial Transplant 1998;13:3184-3188. 3. Dudley J, Afifi E, Gardner A, Tizard EJ, McGraw ME. Polymorphism of the ACE gene in Henoch-Schonlein purpura nephritis. Pediatr Nephrol 2000;14:218-220. 4. Brodkiewicz A, Ciechanowicz A, Urbanska A, et al. The I/D polymorphism of the ACE gene in children with Henoch-Schoenlein purpura. Pol Merkuriusz Lek 2000;8:236-238. 5. Ha CW, Kim JY, Lee JN, Lee JH, Chung WY. The Effect of Angiotensin Converting Enzyme Gene Polymorphism in Children with Henoch-Schonlein Purpura Nephritis. J Korean Pediatr Soc 2002;45:884-890. 6. Zhou J, Tian X, Xu Q. Angiotensin-converting enzyme gene insertion/deletion polymorphism in children with Henoch-Schonlein purpua nephritis. J Huazhong Univ Sci Technolog Med Sci 2004;24:158-161. 7. Choi HJ, Cho HY, Kim EJ, et al. Prognostic Factors in Children with Henoch-Schonlein Purpura Nephritis. J Korean Soc Pediatr Nephrol 2005;9:183-192. |
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