Diabetic Nephropathy

Diabetic nephropathy (DN) is a progressive kidney disease and is characterized clinically by the increased blood pressure, occurrence of albuminuria and a gradual loss of kidney function (1). The morphological changes associated with early phase DN comprise diffuse thickening of the glomerular capillary basement membrane together with the nodular glomerulosclerosis (2). Although the pathophysiology of DN is mainly occur due to hyperglycemia, it is believed to involve a combination of genetic and environmental factors. Crucially, DN is not clinically detectable until significant kidney damage has developed, highlighting the need to identify early-stage biomarkers. Current therapies for DN target renin-angiotensin, complement and coagulation
Gene expression studies suggested that 3 PPAR forms are differentially expressed in the kidney (5, 6). PPAR-gamma (PPARG) mRNA is mainly localized in renal medullary collecting duct with lower expression in renal glomeruli and renal micro vasculature (7). PPARG is involved in renal hemodynamic and water and sodium transport. Further, numerous studies have demonstrated the renoprotective actions of PPARG, such as improved insulin resistance, decreased blood glucose, reduced levels of circulating non-esterified fatty acid and insulin-desensitizing cytokines, increased plasma adiponectin level and lowered blood pressure (8-12). PPARG gene spans more than 100 kb of genomic DNA on 3q25, and harboring a most studied missense mutation resulting in the alanine substitution for proline at codon 12 (Pro12Ala) of the PPARG gene (rs1801282) (13). Although, the mechanisms by which the PPARG Pro12Ala polymorphism contributes to diabetic nephropathy is not yet elucidated completely, several studies have investigated the association between PPARG Pro12Ala polymorphism and diabetic nephropathy risk. The aim of our meta-analysis was to quantitatively summarize the association of PPARG gene Pro12Ala polymorphisms with diabetic