Diabetic Nephropathy Research Paper

Abstract
Diabetic vascular complication is a leading cause of diabetic nephropathy, a progressive increase in urinary albumin excretion coupled with elevated blood pressure leading to declined glomerular filtration and eventually end stage renal failure. There is growing evidence that activated inflammation is contributing factor to the pathogenesis of diabetic nephropathy. Meanwhile, IL-18, a member of the IL-1 family of inflammatory cytokines, is involved in the development and progression of diabetic nephropathy. However, the benefits derived from the current therapeutics for diabetic nephropathy strategies still provide imperfect protection against renal progression. This imperfection points to the need for newer therapeutic agents that have potential to affect primary mechanisms contributing to the pathogenesis of diabetic nephropathy. Therefore, the recognition of IL-18 as significant pathogenic mediators in diabetic nephropathy leaves open the possibility of new potential therapeutic targets.

Introduction

Chronic hyperglycemia induces tissue damage in particular cell types such as mesangial cells in renal glomerulus which contributes to renal pathology in diabetes. High glucose plays a central role in the development and progression of diabetic renal complications via various mechanisms such as increased production of advanced glycation end products, activation of protein kinase C, stimulation of the polyol pathway and enhanced reactive oxygen species generation (Al-Gayyar et al., 2011; Ali et al., 2011; Ali et al., 2008; Elsherbiny et al., 2013; Yamagishi & Imaizumi,