Toxic effects of hyperglycemia-induced advanced glycosylated end produ
cts (AGEs) may explain some vasculopathic complications of diabetes. A
minoguanidine, a known inhibitor of AGE formation, was administered by
gavage to Sprague-Dawley streptozotocin-induced diabetic rats made az
otemic by surgical reduction of renal mass, All rats became hyperglyce
mic. Renal ablation caused renal insufficiency, as evidenced by marked
ly reduced endogenous creatinine clearances at days 7 and 14. Aminogua
nidine-treated rats had significantly (P < 0.04) superior survival to
that of untreated azotemic diabetic rats. We infer from the extended l
ife in a rat model of uremia in diabetic nephropathy that aminoguanidi
ne may prove beneficial in human diabetes. (C) 1997 by the National Ki
dney Foundation, Inc.