Hemoglobin A1c Measurements over Nearly Two Decades: Sustaining Comparable Values throughout the Diabetes Control and Complications Trial and the Epidemiology of Diabetes Interventions and Complications Study

Steffes, Michael W.; Cleary, Patricia A.; Goldstein, David E.; Little, Randie R.; Wiedmeyer, Hsiao Mei; Rohlfing, Curt L.; England, J D; Bucksa, Jean M.; Nowicki, Maren

doi:10.1373/clinchem.2004.042143

Cited by 103 publications

(84 citation statements)

References 19 publications

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“…Other procedures. Each EDIC subject had an annual history, physical examination, electrocardiogram, and laboratory testing, including serum creatinine and A1C, determined as they were during the DCCT (9,10,23). Fasting lipid profiles and 4-h urine collections for measurement of albumin excretion rate and creatinine clearance were obtained in alternate years during the EDIC study (9).…”

Section: Methodsmentioning

confidence: 99%

The Effect of Intensive Glycemic Treatment on Coronary Artery Calcification in Type 1 Diabetic Participants of the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study

et al. 2006

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The Epidemiology of Diabetes Interventions and Complications (EDIC) study, an observational follow-up of the Diabetes Control and Complications Trial (DCCT) type 1 diabetes cohort, measured coronary artery calcification (CAC), an index of atherosclerosis, with computed tomography (CT) in 1,205 EDIC patients at ϳ7-9 years after the end of the DCCT. We examined the influence of the 6.5 years of prior conventional versus intensive diabetes treatment during the DCCT, as well as the effects of cardiovascular disease risk factors, on CAC. The prevalences of CAC >0 and >200 Agatston units were 31.0 and 8.5%, respectively. Compared with the conventional treatment group, the intensive group had significantly lower geometric mean CAC scores and a lower prevalence of CAC >0 in the primary retinopathy prevention cohort, but not in the secondary intervention cohort, and a lower prevalence of CAC >200 in the combined cohorts. Waistto-hip ratio, smoking, hypertension, and hypercholesterolemia, before or at the time of CT, were significantly associated with CAC in univariate and multivariate analyses. CAC was associated with mean HbA 1c (A1C) levels before enrollment, during the DCCT, and during the EDIC study. Prior intensive diabetes treatment during the DCCT was associated with less atherosclerosis, largely because of reduced levels of A1C during the DCCT. Diabetes 55: 3556 -3565, 2006 P atients with type 1 diabetes have a high risk of developing cardiovascular disease (CVD), which in young adulthood can be 10-fold higher than in the general population (1,2). The reasons for this increased risk have not been fully elucidated and can only be partly explained by standard cardiovascular risk factors. Surprisingly, cumulative hyperglycemia has not been shown consistently to be a risk factor for cardiovascular events in type 1 diabetes (3-8).The Diabetes Control and Complications Trial (DCCT)/ Epidemiology of Diabetes Interventions and Complications (EDIC) study provides an opportunity to explore the complex relationships among traditional CVD risk factors, glycemia, and CVD outcomes (9). The DCCT demonstrated the importance of glycemic control in preventing or delaying microvascular complications (10), but it did not reach a clear conclusion with respect to macrovascular complications, owing to the low prevalence of macrovascular disease in the relatively young cohort (11). The long-term EDIC follow-up included assessments of subclinical CVD with measurement of carotid intima-media thickness (IMT) (12,13) and with computerized tomography (CT) of the heart to detect and quantitate calcification in the coronary arteries, a marker of atherosclerosis (14). The EDIC study demonstrated a significant protective effect of prior intensive diabetes therapy, compared with conventional therapy, on the progression of IMT over a 6-year period that was associated with the level of HbA 1c (A1C) (13). Progression of IMT was associated with the level of glycemia (A1C) over time, consistent with some (15), but not all (16,17), reports in type 1 di...

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Section: Methodsmentioning

confidence: 99%

The Effect of Intensive Glycemic Treatment on Coronary Artery Calcification in Type 1 Diabetic Participants of the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study

et al. 2006

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“…Hemoglobin A1c was measured quarterly during the DCCT using HPLC. 22 AER was measured yearly during the DCCT and every other year during EDIC by 4-hour timed urine collection using a fluoroimmunoassay (interassay CV=9.4%). 9 …”

Section: Other Clinical Characteristicsmentioning

confidence: 99%

Longitudinal Changes in Estimated and Measured GFR in Type 1 Diabetes

Sun

Cleary

Lachin

et al. 2014

Journal of the American Society of Nephrology

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Estimation of GFR from serum concentrations of creatinine and cystatin C has been refined using crosssectional data from large numbers of people. However, the ability of the improved estimating equations to identify changes in GFR within individuals over time has not been rigorously evaluated, particularly within the normal range of GFR. In cross-sectional and longitudinal analyses of 1441 participants in the Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications (EDIC) study with type 1 diabetes, we compared GFR estimated from creatinine (eGFR Cr ), cystatin C (eGFR Cys ), or both (eGFR Cr+Cys ) with iothalamate GFR (iGFR), including changes in each over time. Mean (SD) iGFR was 122.7 (21.0) ml/min per 1.73 m 2 . In cross-sectional analyses, eGFR Cr+Cys estimated iGFR with the highest correlation (r=0.48 versus 0.39-0.42), precision, and accuracy. In longitudinal analyses, change in eGFR Cr+Cys best estimated change in iGFR; however, differences between estimates were small, and no estimate accurately classified change in iGFR. Over a median 23 years of follow-up, mean rate of change in eGFR was similar across estimates of eGFR Cr , eGFR Cys , and eGFR Cr+Cys (21.37, 21.11, and 21.29 ml/min per 1.73 m 2 per year, respectively). Associations of BP and hemoglobin A1c with change in eGFR were strongest for eGFR Cys and eGFR Cr+Cys . Together, these results suggest that the addition of cystatin C to creatinine to estimate GFR may improve identification of the causes and consequences of GFR loss in type 1 diabetes, but may not meaningfully improve the tracking of GFR in clinical care. 25: 810-818, 201425: 810-818, . doi: 10.1681 Reduced GFR leads to ESRD and metabolic complications of CKD. Estimation of GFR from serum concentrations of creatinine and cystatin C has been refined using cross-sectional data from large numbers of people. 1 As a result, individuals with reduced GFR and increased risk of adverse clinical outcomes can be more accurately identified within populations. 1,2 However, the ability of the improved estimating equations to identify changes in GFR within individuals over time has not been rigorously evaluated, particularly within the normal range of GFR ($60 ml/min per 1.73 m 2 ). Detecting changes in GFR within individual patients is important to develop, evaluate, and implement strategies to prevent CKD. J Am Soc NephrolIdentifying changes in GFR within individuals may be particularly useful in type 1 diabetes. Patients with type 1 diabetes often have GFR higher than normal early in the course of disease (hyperfiltration). 3 Over many years of follow-up, some of these patients develop overtly reduced GFR (,60 ml/min per 1.73 m 2 ). 4 Tracking GFR during this interval is challenging, because large changes in GFR may cause only small changes in serum creatinine and cystatin C concentrations. In addition, it is now clear that macroalbuminuria (urine albumin excretion$300 mg/d) is not a sensitive marker of early GFR loss. Rather, some patients...

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“…Glycation of lysine residues on Hb molecules would contribute to AGEs formation, besides that of the N-terminal valine of HbA1c, which is well known to be a diagnostic tool for diabetes (19). The reactions for AGEs formation proceed after the attack of a nucleophilic reagent on the carbonyl group of Amadori products.…”

Section: Analysis Of the Structure Of The Glycation Sitementioning

confidence: 99%

The structural feature surrounding glycated lysine residues in human hemoglobin

2011

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Complications derived from diabetes mellitus are caused by nonenzymatic protein glycation at the specific sites. LC/MS/MS was performed for the identification of the tryptic peptides of glycated hemoglobins using glyceraldehyde. After the identification of the glycation or non-glycation site, computer analysis of the structure surrounding the sites was carried out using PDB data (1BZ0). Five glycated lysine residues (Lys-16(α), -56(α), -8(β), -82(β), and -144(β)) and four non-glycated lysine residues (Lys-7(α), -40(α), -99(α), and -132(β)) were identified. The non-glycated lysine residues, Lys-7(α), -40(α), and -132(β), are most likely to form electrostatic interactions with the β

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Hemoglobin A1c Measurements over Nearly Two Decades: Sustaining Comparable Values throughout the Diabetes Control and Complications Trial and the Epidemiology of Diabetes Interventions and Complications Study

Cited by 103 publications

References 19 publications

The Effect of Intensive Glycemic Treatment on Coronary Artery Calcification in Type 1 Diabetic Participants of the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study

The Effect of Intensive Glycemic Treatment on Coronary Artery Calcification in Type 1 Diabetic Participants of the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) Study

Longitudinal Changes in Estimated and Measured GFR in Type 1 Diabetes

The structural feature surrounding glycated lysine residues in human hemoglobin

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