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Volume 2, Issue 1, Pages 10-14 (April 2010)


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Fluctuations in glycosylated hemoglobin (HbA1C) as a predictor for the development of diabetic nephropathy in type 1 diabetic patients

Jocelyn Eid Faresa, Mona Kanaanb, Monique Chaayab, Sami T. AzaraCorresponding Author Informationemail address

Received 28 October 2009; received in revised form 17 December 2009; accepted 20 December 2009. published online 18 January 2010.

Abstract 

Objective

The incidence of diabetic nephropathy is higher in type 1 diabetic patients with associated risk factors. The within individual fluctuations in HbA1C and its effect on the development of nephropathy was not previously studied. The purpose of this study is to examine whether HbA1C fluctuations are a predictor of the development of diabetic nephropathy independent of mean HbA1C and other risk factors.

Methods

One hundred and seventeen patients (64 females and 53 males) were recruited and followed up regularly at least every 3months. The “fluctuations” in HbA1C over time was assessed. HbA1C fluctuation was defined as an increase in HbA1C of more than 2% between two consecutive measurements, or an increase of more than 1% at 2 points in time.

Results

Incipient nephropathy was present in 18 and absent in 99 patients. Mean HbA1C was significantly higher in nephropathy than in non-nephropathy patients. The effect of fluctuations on nephropathy appeared to be more significant in patients with poor metabolic control (HbA1C8%).

Conclusion

T1D patients who have a similar mean HbA1C may progressively behave differently in terms of developing nephropathy, depending on the fluctuations in HbA1C. This effect seems to be more pronounced among those who have higher values of HbA1C.

a Department of Internal Medicine, Division of Endocrinology, American University of Beirut-Medical Center, 3 Dag Hammarskjold Plaza – 8th Floor, New York, NY 10017 2324, USA

b Department of Epidemiology and Population Heath, American University of Beirut, USA

Corresponding Author InformationCorresponding author. Tel.: +1 961 3 234 250; fax: +1 961 1 365 189.

PII: S1877-5934(09)00069-1

doi:10.1016/j.ijdm.2009.12.012


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