Oxidative stress in early diabetic nephropathy: fueling the fire.
Study Goal
The researchers aimed to explore the role of oxidative stress, particularly involving Advanced Glycation End Products, in the pathogenesis and progression of diabetic nephropathy.
Results Summary
The study found that excessive production of Advanced Glycation End Products contributes to oxidative stress and endothelial dysfunction in diabetic nephropathy, but current therapeutic strategies have limited success in addressing these effects.
Population
Patients with diabetic nephropathy, a complication of diabetes mellitus.
Effective Dosage
Not specified
Duration
Not specified
Interactions
None mentioned
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
current therapies to maintain good glycemic control, adequate blood pressure and lipid levels, along with lifestyle measures such as regular exercise, optimization of diet and smoking cessation | decrease | oxidative stress and endothelial cell dysfunction | patients with diabetic nephropathy | - | may help to reduce | #1 |
current therapies to maintain good glycemic control, adequate blood pressure and lipid levels, along with lifestyle measures such as regular exercise, optimization of diet and smoking cessation | decrease | the progression of diabetic nephropathy | patients with diabetic nephropathy | - | may help to retard | #2 |
Diabetic nephropathy is a major microvascular complication of diabetes mellitus and the most common cause of end-stage renal disease worldwide. The treatment costs of diabetes mellitus and its complications represent a huge burden on health-care expenditures, creating a major need to identify modifiable factors concerned in the pathogenesis and progression of diabetic nephropathy. Chronic hyperglycemia remains the primary cause of the metabolic, biochemical and vascular abnormalities in diabetic nephropathy. Promotion of excessive oxidative stress in the vascular and cellular milieu results in endothelial cell dysfunction, which is one of the earliest and most pivotal metabolic consequences of chronic hyperglycemia. These derangements are caused by excessive production of advanced glycation end products and free radicals and by the subjugation of antioxidants and antioxidant mechanisms. An increased understanding of the role of oxidative stress in diabetic nephropathy has lead to the exploration of a number of therapeutic strategies, the success of which has so far been limited. However, judicious and timely use of current therapies to maintain good glycemic control, adequate blood pressure and lipid levels, along with lifestyle measures such as regular exercise, optimization of diet and smoking cessation, may help to reduce oxidative stress and endothelial cell dysfunction and retard the progression of diabetic nephropathy until more definitive therapies become available.