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BACKGROUND The glycation gap has been proposed as an index of nonglycemic determinants of glycated hemoglobin (Hb A1c). We investigated whether it predicts progression of nephropathy in type 2 diabetic patients. METHODS We recorded albumin excretion rate, Hb A1c, and serum fructosamine in 2314 patients over an average of 6.5 years. Hb A1c was regressed on fructosamine by using a repeated-measures longitudinal regression model and data for all visits of all patients; the raw glycation gap gg was calculated at each visit, as measured by Hb A1c minus the value predicted by the regression; and the mean glycation gap (GG) was defined for each patient as the mean of the values for the raw glycation gap (gg) calculated at each visit. The study group was divided into high-, medium- and low-GG groups of equal sizes, which were compared for progression of nephropathy by Cox regression analyses controlling for age, sex, duration of diabetes, initial nephropathy status, therapy, baseline Hb A1c, mean Hb A1c, and mean fructosamine. The design of the study was a retrospective cohort study with follow-up for 6.5 (SD 4.2) years. RESULTS The gg exhibited considerable stability over time. In the high- and medium-GG groups, the risk of progression of nephropathy was respectively 2.5 and 1.6 times that of the low-GG group (P < 0.0001 and P = 0.001, respectively) after adjustment as described above. CONCLUSIONS GG predicts the progression of nephropathy in type 2 diabetic patients independently of fructosamine and even after adjustment for Hb A1c. The joint use of the glycation gap and fructosamine as measures of nonglycemic and glycemic determinants of glycation, respectively, may improve evaluation of the risk of nephropathy and of the glycemic control desirable for the individual patient.

In patients with Type 2 diabetes, the risk of progression of nephropathy increases significantly with HbA(1c) variability, independently of the influence of updated mean HbA(1c) .

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OBJECTIVEThe glycation gap (the difference between measured A1C and the value predicted by regression on fructosamine) is stable and is associated with microvascular complications of diabetes but has not hitherto been estimated within a clinically useful time frame. We investigated whether two determinations 30 days apart suffice for a reasonably reliable estimate if both A1C and fructosamine exhibit stability.RESEARCH DESIGN AND METHODSWe studied 311 patients with type 1 or type 2 diabetes for whom simultaneous measurements of A1C and serum fructosamine had been made on at least two occasions separated by 1 month (t0 and t1). Glycemia was deemed stable if A1C(t1) – A1C(t0) and fructosamine(t1) − fructosamine(t0) were both less than their reference change values (RCVs). Instantaneous glycation gaps [gg(t0) and gg(t1)] and their mean (GG), were calculated using the data from all stable patients for the required regression.RESULTSStable glycemia was shown by 144 patients. In 90% of unstable case subjects, a change in medication was identified as the cause of instability. Among 129 stable patients with an average of eight gg determinations prior to t0, GG correlated closely with the mean of these prior determinations (r2 = 0.902, slope 1.025, intercept −0.038).CONCLUSIONSThe glycation gap can be calculated reliably from pairs of A1C and fructosamine measurements taken 1 month apart if these measurements satisfy the RCV criteria for glycemic control.

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