Interleukin –18 and other inflammatory cytokines as independent predictors of diabetic nephropathy in patients with type 2 diabetes mellitus.

Abstract

Diabetes Mellitus is a very common cause of glomerular disease in adults and is a very common cause of end stage renal failure. The pathogenesis of diabetic nephropathy is not completely understood dispite extensive investigations. Involvement of the kidneys in patients with diabetes mellitus includes not only hyperglycemia, advanced glycosylation products but also activation of proinflammatory cytokines. Data about the relationship of inflammation to nephropathy in type 2 diabetes mellitus are scarce. Our study was conducted to compare levels of interleukin - 18 ( IL- 18), tumor necrosis factor-alpha.( TNF- α ) and interleukin- 6 (IL-6) in serum of diabetic patients with various degrees of nephropathy. The study included 50 patients and 35 normal control subjects presented at Ain Shams University Hospitals. The diabetic subjects were divided into 3groups according to urinary albumin excretion ( UAE): o Group I : included 22 subjects with UAE 300 μg/mg creatinine i.e. diabetic patients with macroalbuminuria. The serum levels of IL–18, TNF- α and IL-6 were measured for the control group to determine the normal values and for all diabetic subjects with various degrees of nephropathy . The results revealed highly significant statistical differences in serum levels of IL-18, TNF-α and IL-6 between the patients and control subjects. In addition, IL-18 levels were increased in diabetic patients with proteinuria as compared with those without proteinuria. Also TNF-α and IL-6 in diabetic patients with microalbuminuria and clinical albuminuria were significantly increased as compared with diabetic patients without albuminuria. These results suggest that serum levels of IL-18, TNF- α and IL-6 may have etiopathogenic roles in diabetic nephropathy and are independent predictors of UAE in type 2 diabetes mellitus. So, in addition to metabolic and hemodynamic factors, it is possible to consider the participation of inflammation on the pathogenesis of diabetic nephropathy.