2006
DOI: 10.1007/s00125-006-0215-6
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Anaemia in diabetes: is there a rationale to TREAT?

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Cited by 80 publications
(60 citation statements)
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References 41 publications
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“…It has been pointed out that the oxygen-erythropoietin feedback, which depends on the hypoxia-sensing system HIF-1␣, is dysregulated in diabetes; microangiopathy and progressive tubulointerstitial fibrosis increase the latency of the erythropoietin system, while production of ROS and hyperglycemia itself stabilize HIF-1␣, blunting erythropoietin response (61). Additionally, we have recently demonstrated that EPC mobilization in diabetes is defective because of HIF-1␣ downregulation (19).…”
Section: Epcs and Diabetic Nephropathymentioning
confidence: 90%
“…It has been pointed out that the oxygen-erythropoietin feedback, which depends on the hypoxia-sensing system HIF-1␣, is dysregulated in diabetes; microangiopathy and progressive tubulointerstitial fibrosis increase the latency of the erythropoietin system, while production of ROS and hyperglycemia itself stabilize HIF-1␣, blunting erythropoietin response (61). Additionally, we have recently demonstrated that EPC mobilization in diabetes is defective because of HIF-1␣ downregulation (19).…”
Section: Epcs and Diabetic Nephropathymentioning
confidence: 90%
“…Indeed, correction of anemia in both diabetic and nondiabetic patients with CKD has been shown to reduce hospitalization rate and hospital stay (32,33). Given the high prevalence of anemia and CKD in our diabetic population, there is a need to conduct interventional studies to examine whether optimization of the internal milieu, including correction of anemia, will reduce cardiovascular and renal risk (34).…”
Section: Discussionmentioning
confidence: 99%
“…Predominant tubulointerstitial disease is associated with damage to the peritubular interstitial cells that produce erythropoietin. As a result, patients with diabetes may be prone to erythropoietin deficiency and are nearly twice as likely to have anemia compared with patients with nondiabetic CKD and comparable eGFR (40). Insulin is a cofactor for parathyroid hormone release; therefore, insulin deficiency and/or resistance may be associated with lower parathyroid hormone levels than in other types of CKD (41), which may predispose patients with DKD to adynamic bone disease.…”
Section: Natural Historymentioning
confidence: 99%