タナカ リョウジロウ   Ryojiro Tanaka
  田中 亮二郎
   所属   川崎医科大学  医学部 臨床医学 小児科学
   職種   特任教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 ACE gene polymorphism in childhood IgA nephropathy: association with clinicopathologic findings.
掲載誌名 正式名:American journal of kidney diseases : the official journal of the National Kidney Foundation
略  称:Am J Kidney Dis
ISSNコード:15236838/02726386
掲載区分国外
巻・号・頁 31(5),pp.774-9
著者・共著者 R Tanaka, K Iijima, R Murakami, M Koide, H Nakamura, N Yoshikawa
発行年月 1998/05
概要 A deletion polymorphism in the angiotensin-converting enzyme (ACE) gene has been reported to be a risk factor for progression to chronic renal failure in immunoglobulin A nephropathy (IgAN). In this study, we investigated the association between ACE gene polymorphism and clinical findings, early biopsy findings such as the extent of mesangial proliferation, focal lesions (capsular adhesions, glomerulosclerosis, and crescents), and the glomerular area in childhood IgAN. Genomic DNA was obtained from 97 patients and control subjects. Gene polymorphisms, consisting of an insertion (I) or deletion (D) of the 287-base pair Alu sequence, were detected using the polymerase chain reaction. The extent of capsular adhesions and glomerulosclerosis was significantly higher in patients with the ID/DD genotypes than in those with the II genotype (ID/DD v II: 8.0%+/-1.4% v 2.5%+/-0.8% [P = 0.017] and 5.1%+/-1.3% v 1.4%+/-0.6% [P = 0.028], respectively). Whereas there was no difference in the extent of mesangial proliferation and crescents between the ID/DD genotypes and the II genotype. Urinary protein excretion at the time of biopsy was significantly greater in patients with the ID/DD genotypes than in those with the II genotype (1.02+/-0.15 g/d/m2 body surface area v 0.56+/-0.13 g/d/m2 body surface area; P = 0.012). These results indicate that ACE gene polymorphism may not influence the extent of mesangial proliferation and crescents that are acute lesions. However, the ID/DD genotypes are associated with chronic lesions, such as capsular adhesions or glomerulosclerosis and urinary protein excretion in childhood IgAN.
DOI 10.1016/s0272-6386(98)70045-9
PMID 9590186