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.