New evidence shows that systemic and intrarenal hemodynamic abnormalities are major factors in the initiation and progression of diabetic nephropathy. Genetic predisposition to elevated systemic blood pressure may contribute to its development. Glomerular vasodilation and hyperfiltration, mediated in part by prostaglandins, may play a role in glomerula damage early in the course of diabetes, but clinical studies are limited. The development of more sensitive assays for albuminuria now allows early diagnosis of incipient nephropathy in the 'microalbuminuria' phase. Treatment during this phase with antihypertensive agents, including angiotensin-converting enzyme inhibitors, or with dietary protein restriction, can decrease the degree of albuminuria, but data on their long-term effects on disease progression are limited. In hypertensive patients with established clinical diabetic nephropathy characterized by proteinuria in excess of 0.3 to 0.5 g/d, antihypertensive therapy has a major impact on delaying renal failure. Modalities that lower both systemic and intraglomerular pressure may be more beneficial in preserving renal function than those that primarily lower systemic pressure. Any therapeutic intervention should be monitored meticulously to establish its efficacy and safety in the individual patient. Therapy specifically directed against hemodynamic abnormalities throughout the course of diabetic renal disease may significantly delay and decrease the negative impact of this diabetic complication on survival and quality of life.
|Original language||English (US)|
|Number of pages||19|
|Journal||Annals of Internal Medicine|
|State||Published - 1989|
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