C-106T Polymorphism in Promoter of Aldose Reductase Gene Is a Risk Factor for Diabetic Nephropathy in Type 2 Diabetes Patients with Poor Glycaemic Control

Vol. 99, No. 3, 2005

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Original Paper

C-106T Polymorphism in Promoter of Aldose Reductase Gene Is a Risk Factor for Diabetic Nephropathy in Type 2 Diabetes Patients with Poor Glycaemic Control
Katarzyna Gosek, Dariusz Moczulski, Ewa Zukowska-Szczechowska, Wladyslaw Grzeszczak

Department and Clinic of Internal Medicine, Diabetology and Nephrology, Silesian School of Medicine, Zabrze, Poland

Address of Corresponding Author

Nephron Exp Nephrol 2005;99:e63-e67 (DOI: 10.1159/000083209)

Key Words

Type 2 diabetes
Diabetic nephropathy
Aldose reductase
C-106T polymorphism

Abstract

Background: Excessive flux through the polyol pathway has long been thought to be involved in the pathogenesis of diabetic microvascular complications. Aldose reductase (AR) is the first and rate-limiting enzyme in the pathway that catalyses the reduction of glucose to sorbitol. A frequent C-106T polymorphism in the promoter of the AR gene has been described, which may change the expression of the gene. The aim of the study was to examine if the C-106T polymorphism was associated with diabetic nephropathy. Material and Methods: We collected 444 patients with type 2 diabetes and divided them into three groups according to the renal status: 162 patients with normoalbuminuria, 153 with microalbuminuria and 129 with persistent proteinuria. Each subject was genotyped for the C-106 polymorphism using the PCR-based RFLP protocol. Results: When the whole study population was analysed, no distortion in the genotype frequency among the study groups was observed. When we stratified the study population by HbA1c we found that in patients with HbA1c 9% (median) the CT and TT genotypes were more frequent in patients with diabetic nephropathy (proteinuria and microalbuminuria) than those with normoalbuminuria (OR 2.04, 95% CI 1.12-3.74). Conclusion: The C-106T polymorphism in the AR gene is a risk factor for development of diabetic nephropathy in type 2 diabetes in patients with poor glycaemic control.

Author Contacts

Katarzyna Gosek, MD, PhD
Department and Clinic of Internal Medicine
Diabetology and Nephrology
ul. 3-go Maja 13-15, PL-41-800 Zabrze (Poland)
Tel. +48 32 2712511, Fax +48 32 2714617, E-Mail kasiagos@poczta.onet.pl

Article Information

Received: January 24, 2004
Accepted: August 5, 2004
Published online: January 5, 2005
Number of Print Pages : 5
Number of Figures : 0, Number of Tables : 3, Number of References : 25

Medline Abstract (ID 15637423)

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