Hyperglycemia, the most obvious metabolic abnormality in diabetes, is the primary casual factor responsible for the development of diabetic microvascular complications. There is considerable evidence linking hyperglycemia with the accelerated formation of irreversible nonenzymatic advanced glycosylation end products (AGEs), which subsequently accumulate in vessel wall proteins. The development of long-term vascular complications associated with diabetes appears to be related to the accumulation of these AGEs. Compounds that inhibit the development of AGE formation prevent complications in animal models and, therefore, may prove useful in reducing chronic diabetes-related complications in patients.