Abstract
Most physicians accept that hyperglycemia makes an important contribution to the complications of diabetes mellitus involving small and large vessels, but whether hyperglycemia alone is sufficient to explain diabetic vascular disease remains controversial. Epidemiologic evidence suggests that the end-organ response to exposure to diabetes, defined as the duration of hyperglycemia multiplied by its degree, differs in different vascular beds. Given time, retinopathy appears to develop in virtually all patients with insulin-dependent diabetes mellitus (IDDM), but this is not the case for nephropathy or cardiovascular disease.1 The cumulative risk of albuminuria in patients with IDDM is about 35 percent, no matter . . .