Chronic hyperglycemia results in a non-enzymatic glycation of proteins, and produces Amadori products, such as glycated albumin (GA), glycosylated hemoglobin (HbA1c), and fructosamine. In current clinical practice, long-term glycemic control is assessed by quarterly measurements of HbA1c. Since the degree of hemoglobin glycosylation depends not only on the level of glycemic control, but also on the lifespan of red blood cells, patients with hemoglobin disorders or anemia of any cause may have erroneous HbA1c levels, and consequently receive insufficient treatment. Patients with chronic kidney disease (CKD) often suffer from various types of anemia, and consequently, they are frequently treated with iron and/or erythropoietin therapy or frequent blood transfusion. Thus, serum GA is a potentially useful glycemic index in diabetic patients with CKD, since it is not influenced by anemia and associated treatments. GA may also reflect the status of blood glucose more rapidly (2-3. weeks) than HbA1c (2-3. months), and is beneficial in those with wide variations in blood glucose or at higher risk for hypoglycemia. If clinical investigations support its utility, it may be applicable as a screening tool for all patients with diabetes during routine health examinations. Serum GA levels are also associated with AGE-related fluorescence and the number of glycation sites, and it may influence the structural and functional changes inalbumin. Since end-stage renal disease is an extreme microvascular complication of diabetic nephropathy, CKD patients with diabetes should be carefully managed to prevent disease progression. In this review, the clinical aspects of GA were discussed, including a comparison of GA with other glycated proteins, the utility and limitations of GA as a glycemic index, its influence on the therapeutic effects of hypoglycemic agents, its correlations with vascular complications, and its potential role in pathogenesis, specifically in diabetic patients with CKD.
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