Literature DB >> 9706125

Nephropathy and hypertension in diabetes.

J B Marks1, P Raskin.   

Abstract

The treatment of the patient with diabetes, with or without hypertension, is complex and challenging. Hyperglycemic treatment should ideally not only control blood glucose, but also prevent the chronic complications and associated metabolic derangements that can lead to increased morbidity and mortality. Hypertensive treatment should not only decrease blood pressure, but also reduce the risk of macrovascular and microvascular disease. The use of antihypertensive agents that improve insulin resistance, dyslipidemia, glycemic control, and nephropathy is preferred whenever possible. The real key to success in the care of the hypertensive diabetic patient is adequate screening and appropriate, early treatment. Currently, there is ample evidence to support the use of intensive management with the goal of near-normalization of blood glucose levels in most patients with diabetes. Similarly, aggressive treatment of hypertension is the current standard. Accomplishing these goals helps to prevent the development of chronic diabetic complications, including nephropathy. ESRD need not be the inevitable outcome for individuals with early diabetic nephropathy. Interventions currently available that are targeted at the known modifiable risk factors underlying the development and progression of diabetic nephropathy offer the best hope for reducing the incidence and severity of this complication. Prevention of the complications of diabetes, including nephropathy, must be the goal for the future on behalf of all those who now have diabetes.

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Year:  1998        PMID: 9706125     DOI: 10.1016/s0025-7125(05)70028-6

Source DB:  PubMed          Journal:  Med Clin North Am        ISSN: 0025-7125            Impact factor:   5.456


  4 in total

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3.  Collagen I induction by high glucose levels is mediated by epidermal growth factor receptor and phosphoinositide 3-kinase/Akt signalling in mesangial cells.

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Journal:  Diabetologia       Date:  2007-07-11       Impact factor: 10.122

4.  Fenofibrate attenuated glucose-induced mesangial cells proliferation and extracellular matrix synthesis via PI3K/AKT and ERK1/2.

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  4 in total

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