Role of GLUT1 gene in susceptibility to diabetic nephropathy in type 2 diabetes

Citation
W. Grzeszczak et al., Role of GLUT1 gene in susceptibility to diabetic nephropathy in type 2 diabetes, KIDNEY INT, 59(2), 2001, pp. 631-636
Citations number
27
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
KIDNEY INTERNATIONAL
ISSN journal
00852538 → ACNP
Volume
59
Issue
2
Year of publication
2001
Pages
631 - 636
Database
ISI
SICI code
0085-2538(200102)59:2<631:ROGGIS>2.0.ZU;2-T
Abstract
Background The XbaI polymorphism in the glucose transporter GLUT1 gene has been implicated in the development of diabetic nephropathy in Chinese type 2 diabetes patients. Methods. To examine whether the XbaI polymorphism is involved in the develo pment of diabetic nephropathy in Caucasian type 2 diabetes patients, a larg e case control study was performed. The study group of 444 patients with ty pe 2 diabetes consisted of three subgroups: 162 patients with normoalbuminu ria (only patients with duration of type 2 diabetes of at least 10 years af ter diagnosis); 150 with microalbuminuria; and 132 subjects with persistent proteinuria or chronic renal failure (CRF). The polymerase chain reaction (PCR)-based genotyping of the XbaI polymorphism was performed in each subje ct. Results. The genotype distribution in the subgroups showed an increased fre quency of the (+/+) genotype in patients with microalbuminuria (41%; OR 1.4 0, 95% CI, 0.89 to 2.24) and proteinuria/CRF (47%; OR 1.82, 95% CI, 1.13 to 2.93, P = 0.013) when compared with normoalbuminuria (33%). No difference in the genotype distribution was observed between type 2 diabetes patients and healthy controls. Conclusions. The results of this study in Caucasian patients with type 2 di abetes indicate that the XbaI(-) allele in the GLUT1 gene protects against the development of diabetic nephropathy. Our results are in contrast to the case control study in Chinese patients with type 2 diabetes in which the p resence of the XbaI(-) allele appeared to have a strong association with th e development of diabetic nephropathy.