A-20C angiotensinogen gene polymorphism and proteinuria in childhood IgA nephropathy

Byline: Koichi Nakanishi (1), Mayumi Sako (1), Nahoko Yata (1), Noriyuki Aoyagi (1), Kandai Nozu (2), Ryojiro Tanaka (2), Kazumoto Iijima (3), Norishige Yoshikawa (1,4) Keywords: Promoter; Urinary protein excretion; Heavy proteinuria; Polymerase chain reaction; Restriction fragment length polymorphism Abstract: We have previously reported that the TT genotype of the angiotensinogen gene and the ID/DD genotype of the angiotensin-converting enzyme gene are associated with increased severity of proteinuria in IgA nephropathy in Japanese children. Recently it was reported that polymorphism at -20 from adenine to cytosine in the angiotensinogen gene, increasing the level of this transcript, was associated with the progression of renal dysfunction in adult IgA nephropathy. We therefore investigated whether this polymorphism is involved in IgA nephropathy in Japanese children. We identified this polymorphism in 105 children with IgA nephropathy and 119 healthy adults using polymerase chain reaction/restriction fragment length polymorphism analysis. At the time of biopsy, all patients had normal blood pressure and renal function. There were no differences in the genotypes and allele frequencies of this polymorphism between patients with IgA nephropathy and controls. The number of patients with the AC/CC genotype showing heavy proteinuria (aSS1.0 g/day per m.sup.2 body surface area) at biopsy was significantly higher than that with the AA genotype (P=0.039, chi-squared test). The AC/CC genotype of this polymorphism may be associated with an increased severity of proteinuria, suggesting that this polymorphism may play a significant role in the progression of IgA nephropathy in Japanese children. Author Affiliation: (1) Department of Pediatrics, Wakayama Medical University, Wakayama-City, Wakayama, Japan (2) Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Hyogo, Japan (3) Department of Nephrology, National Center for Child Health and Development, Setagaya, Tokyo, Japan (4) Department of Pediatrics, Wakayama Medical University, Kimiidera 811--1, Wakayama City, Wakayama 641--8510, Japan Article History: Registration Date: 17/10/2003 Received Date: 28/04/2003 Accepted Date: 29/09/2003 Online Date: 28/11/2003