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Given the crucial role of elevated blood pressure (BP) in the progression of diabetic nephropathy, the study of the diurnal variation in BP in diabetes is a surprisingly late phenomenon. It is well documented that the normal night-time drop in BP is reduced in patients with increased urinary albumin excretion (UAE) and in patients with autonomic neuropathy (1). Several recent studies have demonstrated an association between autonomic neuropathy, reduced night-time fall in BP and elevated UAE (2, 3).
The question of a possible causative role of autonomic neuropathy in the development of diabetic nephropathy has naturally arisen (2, 3) and was actually coined 10 years ago (4, 5). The proposed pathogenic link is a higher BP burden at night which is more readily transmitted to glomeruli because of renal vasodilation. If true, ambulatory BP monitoring could identify normoalbuminuric patients at risk of progressing to microalbuminuria as those with a disturbed
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