Protective role of renal nerves in the development of diabetic nephropathy.

Although a significant correlation between the stage of nephropathy and severity of autonomic neuropathy has been demonstrated in diabetes, the mechanism of interaction between these complications is not clear. I studied the role of the renal sympathetic nerves in the development of microalbuminuria in streptozotocin-induced diabetic rats. Sprague-Dawley rats were assigned randomly to one of four groups: 1) non-diabetic sham operated group, 2) non-diabetic renal denervated group, 3) diabetic sham operated group, and 4) diabetic renal denervated group (n = 6 in each group). After recovery of renal denervation and sham operation, diabetes was induced by streptozotocin. Throughout 6 wk of the experiment, diabetes was moderately controlled with ultralente insulin (plasma glucose = 10-24mM). Urinary albumin excretion rose throughout the experiment in all groups, although the rate of increase varied between groups. Among diabetic rats, albuminuria was 3.5 fold higher in renal denervated rats than sham-operated rats in the 6th wk. Among denervated rats, diabetic rats excreted 4.9 fold higher albumin than non-diabetic rats at the end of experiment. Thus, renal denervation appears to exacerbate the progress of diabetic nephropathy in streptozotocin treated rats as judged through assessment of urinary albumin excretion. This suggests that the renal nerves may provide some protection against the progression of diabetic nephropathy. Loss of this protective role may be one mechanism by which diabetic autonomic dysfunction may aggravate the progression of diabetic nephropathy.