Abstract
Glycated hemoglobin (HbA(1C)) is considered clinically useful for assessing long-term integrated control of blood glucose in diabetes. However, an increased HbA(1C) concentration has been documented in chronic renal failure (CRF) patients without any history of diabetes. Collective evidences reveal that lipid peroxidation (MDA) can modulate protein glycation. We evaluated the relationship between glycated hemoglobin (HbA(1C)) and lipid peroxidation in non-diabetic CRF patients. Twenty-eight nondiabetic CRF and 23 age- and sex-matched healthy subjects were enrolled for this study. Plasma urea, creatinine, lipid peroxides, fasting glucose and HbA(1C) were analyzed in both the groups. The in-vitro effect of MDA on glycation of hemoglobin was studied by incubating healthy erythrocytes with either 5 or 50 mmol/l glucose concentration. The percentage of HbA(1C) concentrations and plasma malondialdehyde (MDA) were significantly increased in CRF patients compared to control subjects. When the effects of uremia and blood glucose on the concentration of HbA(1C) was refuted by partial correlation analysis, MDA was found to be a significant determinant of HbA(1C) (r=0.41, p=0.04) in patients with renal failure. In-vitro incubation of RBC with glucose along with MDA was found to enhance the process of hemoglobin glycation. Our results suggest that lipid peroxidation per se can contribute to glycation of hemoglobin, warranting extra-precaution in interpreting HbA(1C) as a measure of glycemic control in CRF.
Published Version
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