Pathophysiological mechanisms of anemia in diabetic nephropathy
Journal Title: Αρχεία Ελληνικής Ιατρικής - Year 2013, Vol 30, Issue 5
Abstract
Diabetes mellitus (DM) is recognized as an epidemic in modern society. It is a syndrome characterized by impaired glucose metabolism, with either decreased or insufficient production of insulin, or increased resistance of the tissues to the action of insulin. The vascular complications of DM are classified as microvascular (diabetic retinopathy, nephropathy and neuropathy) and macrovascular (heart disease and hypertension, peripheral vascular disease and stroke). Diabetic nephropathy (DN) is a leading cause of chronic kidney disease (CKD) in both patients before initiation of dialysis (CKD stages II, III, IV), and those receiving dialysis (CKD stage V). Normochromic normocellular anemia is known to be a frequent complication of CKD, where the primary etiology is decreased production of erythropoietin by the kidney. The severity of anemia is proportional to the stage of CKD, but anemia may be observed before active renal involvement is apparent (i.e., proteinuria, impaired renal function). In addition, anemia in patients with DM and renal disease occurs earlier and in greater severity than in patients with CKD of the same stage but with a different primary renal disease. In addition to iron, vitamin B12 and folic acid deficiency, poor nutrition, secondary hyperparathyroidism, blood loss and malignancy may be involved in the pathogenesis of anemia in DM. Several other, less well known causes and interrelated mechanisms, such as ultrafiltration, proteinuria, chronic inflammation, damage of interstitial kidney tissue, autonomic neuropathy, the uremic toxins, the renin-angiotensin system, increased tubular sodium reabsorption and disorders of erythrocytes are also implicated in the pathogenetic process. This is an overview of the main mechanisms involved in the onset of anemia in these patients.
Authors and Affiliations
M. PAPPA, E. DOUNOUSI, K. KATOPODIS
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