Abstract
We studied the effect of aminoguanidine, an inhibitor of advanced glycation product formation, on albuminuria in chronically diabetic spontaneously hypertensive rats. At the time of killing, there was no statistically significant difference in blood glucose concentration between the treated and untreated diabetic animals (18.2 +/- 0.69 mmol/l), nor was there any difference among the non-diabetic, diabetic untreated, and diabetic treated rats with respect to blood pressure (169 +/- 6.9 mm Hg). However, non-diabetic hypertensive animals had a mean quantitative 24-h urinary albumin excretion of 28 +/- 2 mg albumin/24-h, while untreated diabetic hypertensive animals averaged nearly four times that amount (106 +/- 3 mg albumin/24 h). Without affecting blood pressure, aminoguanidine treatment of diabetic hypertensive animals decreased the diabetic-associated elevation in urinary albumin excretion by 75% (48 +/- 2 mg/24 h). These data suggest than inhibition of advanced glycation product formation ameliorates the glomerular dysfunction caused by chronic hyperglycaemia.
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