ACE GENE POLYMORPHISM IN CHILDHOOD IGA NEPHROPATHY - ASSOCIATION WITHCLINICOPATHOLOGICAL FINDINGS

A deletion polymorphism in the angiotensin-converting enzyme (ACE) gen e has been reported to be a risk factor for progression to chronic ren al failure in immunoglobulin A nephropathy (IgAN). In this study, we I nvestigated the association between ACE gene polymorphism and clinical findings, early biopsy findings such as the extent of mesangial proli feration, focal lesions (capsular adhesions, glomerulosclerosis, and c rescents), and the glomerular area in childhood IgAN. Genomic DNA was obtained from 97 patients and control subjects. Gene polymorphisms, co nsisting of an insertion (I) or deletion (D) of the 287-base pair Alu sequence, were detected using the polymerase chain reaction. The exten t of capsular adhesions and glomerulosclerosis was significantly highe r in patients with the ID/DD genotypes than in those with the II genot ype (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 n o difference in the extent of mesangial proliferation and crescents be tween the ID/DD genotypes and the II genotype. Urinary protein excreti on at the time of biopsy was significantly greater in patients with th e ID/DD genotypes than in those with the II genotype (1.02 +/- 0.15 g/ d/m(2) body surface area v 0.56 +/- 0.13 g/d/m(2) body surface area; P = 0.012). These results indicate that ACE gene polymorphism may not i nfluence the extent of mesangial proliferation and crescents that are acute lesions. However, the ID/DD genotypes are associated with chroni c lesions, such as capsular adhesions or glomerulosclerosis and urinar y protein excretion in childhood IgAN. (C) 1998 by the National Kidney Foundation, Inc.