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• W1963587256 abstract "Tumor necrosis factor-α gene expression in diabetic nephropathy: Relationship with urinary albumin excretion and effect of angiotensin-converting enzyme inhibition.BackgroundThe pathogenic mechanisms and molecular events involved in the development and progression of diabetic nephropathy (DN) are not completely known. Recent data indicate that diabetes includes an inflammatory component that is related to diabetic complications. Tumor necrosis factor (TNF)-α, a cytokine with mainly proinflammatory activity, may be synthesized by renal cells. Our objective was to analyze intrarenal TNF-α gene expression and its relationship with urinary albumin excretion (UAE). We also investigated the effect of inhibition of angiotensin-converting enzyme on TNF-α expression and UAE.MethodsStreptozotocin-induced diabetic rats received either no treatment or an angiotensin-converting enzyme inhibitor (enalapril). After eight weeks, renal expression of TNF-α was evaluated by real-time polymerase chain reaction.ResultsRenal cortical messenger RNA levels of TNF-α increased significantly and were twice as high in diabetic rats than in nondiabetic control rats. Enalapril administration nearly completely abolished the increase in TNF-α messenger RNA expression to the level observed in control rats. UAE was significantly correlated with urinary levels of TNF-α (r = 0.68, P < 0.05) and with renal TNF-α expression (r = 0.51, P < 0.05).ConclusionDN was associated with increased renal expression of TNF-α and UAE. Enalapril administration prevented this enhanced expression of TNF-α and decreased urinary cytokine excretion and albuminuria. These data provide a novel insight into the pathogenic mechanisms of DN, and support the hypothesis that inflammatory mechanisms may play a significant role in the development and progression of renal injury secondary to diabetes mellitus. Tumor necrosis factor-α gene expression in diabetic nephropathy: Relationship with urinary albumin excretion and effect of angiotensin-converting enzyme inhibition. The pathogenic mechanisms and molecular events involved in the development and progression of diabetic nephropathy (DN) are not completely known. Recent data indicate that diabetes includes an inflammatory component that is related to diabetic complications. Tumor necrosis factor (TNF)-α, a cytokine with mainly proinflammatory activity, may be synthesized by renal cells. Our objective was to analyze intrarenal TNF-α gene expression and its relationship with urinary albumin excretion (UAE). We also investigated the effect of inhibition of angiotensin-converting enzyme on TNF-α expression and UAE. Streptozotocin-induced diabetic rats received either no treatment or an angiotensin-converting enzyme inhibitor (enalapril). After eight weeks, renal expression of TNF-α was evaluated by real-time polymerase chain reaction. Renal cortical messenger RNA levels of TNF-α increased significantly and were twice as high in diabetic rats than in nondiabetic control rats. Enalapril administration nearly completely abolished the increase in TNF-α messenger RNA expression to the level observed in control rats. UAE was significantly correlated with urinary levels of TNF-α (r = 0.68, P < 0.05) and with renal TNF-α expression (r = 0.51, P < 0.05). DN was associated with increased renal expression of TNF-α and UAE. Enalapril administration prevented this enhanced expression of TNF-α and decreased urinary cytokine excretion and albuminuria. These data provide a novel insight into the pathogenic mechanisms of DN, and support the hypothesis that inflammatory mechanisms may play a significant role in the development and progression of renal injury secondary to diabetes mellitus." @default.
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• W1963587256 date "2005-12-01" @default.
• W1963587256 modified "2023-10-15" @default.
• W1963587256 title "Tumor necrosis factor-α gene expression in diabetic nephropathy: Relationship with urinary albumin excretion and effect of angiotensin-converting enzyme inhibition" @default.
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• W1963587256 doi "https://doi.org/10.1111/j.1523-1755.2005.09918.x" @default.
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