Abstract

Diabetes mellitus is a well established risk factor for cardiovascular diseases (CVD). In addition, a significant proportion of diabetic patients go on to develop nephropathy. Moreover, the presence of nephropathy further increases the risk of CVD in patients with all stages of diabetic nephropathy, including microalbuminuria, macroalbuminuria, and renal failure. The fibrogenic cytokine transforming growth factor beta (TGF-β) and the vascular endothelial growth factor (VEGF) are implicated in the development of cardinal features of diabetic nephropathy, namely, mesangial expansion and albuminuria, respectively. The pathogenesis of CVD in diabetes is multifactorial and can be affected by metabolic factors, such as oxidative stress, glycoxidation, procoagulant states, and inflammation. Furthermore, endothelial dysfunction may lead to simultaneous development and progression of renal and cardiac pathology in diabetes. The risk of microvascular complications can be reduced by intensive glycemic control, whereas cardiovascular benefit is less clear. Intensified intervention involving other vascular risk factors, such as hypertension and dyslipidemia, demonstrated benefits in terms of both macrovascular and microvascular complications. In addition, treatment with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists is associated with a significant reduction in the risk for renal disease progression in diabetes, which parallels the reduced cardiovascular risk. Moreover, changes in microalbuminuria translate into parallel changes in renal and cardiovascular risk. Nephropathy in diabetic patients is, therefore, important in determining the risk for and outcomes from CVD, the improved understanding of the pathogenesis of renal and vascular disease in diabetes, and as a crucial factor in planning a comprehensive treatment approach to reducing CVD morbidity and mortality in diabetic patients.

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