Anemia And Extrarenal Microvascular Disease

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Several lines of evidence suggest that anemia may influence the course of extrarenal microvascular disease in diabetes. Anemia is associated with an increased risk of background and proliferative retinopathy in patients with diabetes. Given that renal disease and retinopathy are closely associated, it is perhaps not surprising to see an increased prevalence of anemia in patients with more aggressive microvascular disease. However, anemia may also have a direct effect on the development and progression of diabetic retinal disease. Anemia may act to accelerate diabetic retinopathy by promoting retinal hypoxia and macularedema (26). This may be mediated by VEGF, which is a potent stimulus to new vessel formation and increased capillary permeability (27). Consistent with this hypothesis, a few small studies have demonstrated that correction of anemia in patients with diabetes may be associated with a reduction in macular hard exudates (28,29) and edema (30). However, further interventional studies are required to determine if anemia is causally related to diabetic retinopathy.

Similar considerations apply to the association of anemia with DN. Endoneural hypoxia, owing to decreased microvascular blood flow and altered vascular permeability, is observed early in the course of diabetes and the resultant ischemia plays a role in the progressive DN. Factors that exacerbate hypoxia are known to accelerate nerve injury in diabetes and there is evidence that erythropoietin itself has neuropro-tective and neurotrophic effects in experimental diabetes (31). In diabetic patients with anemia and polyneuropathy, erythropoietin therapy has been associated with improvements in motor nerve conduction velocity but no correlation was found between the increase in Hb and improvement in nerve function (32). This raises the possibility that erythropoietin may have a direct impact on microvascular complications, independent of red cell formation. For instance, erythropoietin has been shown to have proangio-genic properties (33) and also to protect vascular endothelial cells and smooth muscle cells against apoptosis (34,35). It follows that the pleiotropic effects of erythropoietin may promote new vessel formation and limit vascular injury in peripheral nerves, kidneys, and the heart in addition to correcting anemia.

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