Abstract
Unlike atheromatous deposits in the larger vessels, the thickening of the basement membrane in the renal and retinal microvasculature of diabetic patients has no readymade metabolic explanation. Ashton 1 attributed these changes to tissue hypoxia caused by reduced blood flow. Spiro 2 ascribed them to deposition of protein-bound carbohydrate, formed in excess by the diversion of glucose to glycoprotein synthesis. Impressed by the beneficial effect of pituitary ablation on diabetic retinopathy, Lundbaek et al 3 sought to implicate the excessive secretion of growth hormone. Incorporating some aspects of these theories into a three-in-one concept, Ditzel 4 hypothesizes that diabetic microangiopathy is a result of diminished tissue oxygenation, which is due less to reduced blood flow than to diminished release of oxygen from the hemoglobin molecule, as reflected in the right shift of the oxygen dissociation curve. This unloading defect could be explained by an increase in hemoglobin A1a-c (fast hemoglobin),
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