SLC2A1 Variants and Diabetic Nephropathy
Cells damaged by hyperglycemia are unable to downregulate glucose entrance in presence of high extracellular glucose resulting in intracellular activation of deleterious biochemical pathways. Expression of GLUT-1, the major glucose transporter in mesangial cells, is increased and participates in the induction of diabetic nephropathy. Variants in the gene encoding GLUT-1 (SLC2A1) have been associated to this diabetic complication. The aim of this study was to test whether polymorphisms in SLC2A1 confer susceptibility to diabetic nephropathy in Brazilian type 1 diabetes patients.
|Study Design:||Observational Model: Case-Only
Time Perspective: Cross-Sectional
|Official Title:||Association of Single Nucleotide Polymorphisms in the Gene Coding GLUT-1 and Diabetic Nephropathy in Brazilian Patients With Type 1 Diabetes Mellitus|
- Plasmatic Creatinine [ Time Frame: Two years ] [ Designated as safety issue: No ]
Biospecimen Retention: Samples With DNA
|Study Start Date:||October 2004|
|Study Completion Date:||October 2012|
|Primary Completion Date:||October 2012 (Final data collection date for primary outcome measure)|
Withou Diabetic Nephropathy
Patients who have persistent normoalbuminuria (<30 mg/g creatinine or <20 μg/min).
Patients who have persistent microalbuminuria (30-300 mg/g creatinine or 20-200 μg/min).
Overt Diabetic Nephropathy
Patients who have persistent macroalbuminuria (>300 mg/g creatinine or >200 µg/min), proteinuria (>500 mg/24 h) or renal replacement therapy.
In this study, 449 patients, included between October 2004 and October 2012, were sorted into three groups according to diabetic nephropathy stages: without (persistent normoalbuminuria, n=248), incipient (microalbuminuria, n=82) and overt diabetic nephropathy (macroalbuminuria or proteinuria or renal replacement therapy, n=119). Measurements of urinary albumin-to-creatinine ratio (ACR) or urinary albumin excretion rate (UAER) were used to define DN: patients with persistent normoalbuminuria (<30 mg/g creatinine or <20 μg/min) were classified as without DN (n=248); patients presenting persistent microalbuminuria (30-300 mg/g creatinine or 20-200 μg/min) were classified as having incipient DN (n=82); and patients presenting persistent macroalbuminuria (>300 mg/g creatinine or >200 µg/min), proteinuria (>500 mg/24 h) or renal replacement therapy were classified as having overt DN (n=119). Genotyping of polymorphisms was performed by Real Time PCR using fluorescent -labelled probes.
|Faculdade de Medicina da USP|
|São Paulo, SP, Brazil, 01246-000|
|Principal Investigator:||Maria L Côrrea-Giannela, Doctor||Hospital Clínicas/Faculdade de Medicina da USP|