The relationship between HbA(1c) and GA% differs in diabetic patients with end-stage renal disease who perform either PD or HD compared to those without nephropathy. HbA(1c) significantly underestimates glycemic control in peritoneal and hemodialysis patients relative to GA%.
SummaryBackground and objectives Relative to hemoglobin (Hb) A 1c , glycated albumin (GA) more accurately reflects glycemic control in patients with diabetes mellitus and ESRD. We determined the association between GA, HbA 1c , and glucose levels with survival and hospitalizations in diabetic dialysis patients.Design, setting, participants, & measurements Quarterly GA levels were measured for up to 2.33 years in 444 prevalent patients with diabetes and ESRD. Proportional hazard time-dependent covariate models were computed with adjustment for demographic characteristics, comorbidities, and laboratory variables. Similar analyses were performed for available HbA 1c and monthly random serum glucose determinations. ResultsThe participants were 53% male, 54% African American, 43% Caucasian, 90% on hemodialysis, with a mean (SD) age of 62 (12) years and median follow-up duration of 2.25 years. Mean Ϯ SD GA and HbA1c were 21.5% Ϯ 6.0% (median 20.4%), and 6.9% Ϯ 1.6% (median 6.6%), respectively. There were 156 deaths during the observation period. In best-fit models, predictors of death included increasing GA, increasing age, presence of peripheral vascular disease, decreasing serum albumin, and decreasing hemoglobin concentrations. HbA 1c and random serum glucose concentrations were not predictive of survival. Increasing GA levels were associated with hospitalization in the 17 days after measurement, whereas HbA 1c was not. ConclusionsIn contrast to the HbA 1c and random serum glucose values, GA accurately predicts the risk of death and hospitalizations in patients with diabetes mellitus and ESRD. The GA assay should be considered by clinicians who care for patients with diabetes on dialysis.
Background: Relative to hemoglobin A1c (HbA1c), glycated albumin (GA) more accurately reflects recent glycemic control in diabetic patients on hemodialysis and peritoneal dialysis. These assays have yet to be compared in patients with advanced chronic kidney disease (CKD). Methods: HbA1c and GA were simultaneously measured in 303 diabetic subjects: 70 with CKD prior to dialysis (CKD-stage 4), 184 with CKD after transplantation (TXP-stage 3) and 49 non-nephropathy controls. Results: Mean estimated GFR was 76, 46 and 26 ml/min in controls, TXP-3 and CKD-4 cases, respectively. Mean (SD) HbA1c (%) and GA (%) concentrations were 7.30 (1.40) and 16.8 (4.9) in controls, 7.28 (1.66) and 21.5 (6.4) in CKD-4 cases, and 7.21 (1.62) and 21.2 (5.5) in TXP-3 cases, respectively. The GA:HbA1c ratio differed significantly between non-nephropathy controls and both groups of CKD patients (both p < 0.001), but not between CKD-4 and TXP-3 cases (p = 0.92). The glucose:HbA1c ratio was inversely associated with GFR in all 254 nephropathy cases (r = –0.13; p = 0.04), while glucose:GA did not vary significantly based upon GFR (r = –0.08; p = 0.24). Conclusions: The relationship between glycated albumin and HbA1c is influenced by the presence of reduced GFR in diabetic patients with CKD. The accuracy of the HbA1c assay in diabetic subjects with severe nephropathy requires further investigation, although HbA1c performs relatively well with milder CKD.
Background: The utility of glycated hemoglobin (HbA1c) and glycated albumin (GA) in diabetic dialysis patients remains unknown. GA was previously associated with all-cause hospitalization and patient survival. Relationships between GA, HbA1c, and casual plasma glucose (PG) with cause-specific cardiovascular (CV) disease, infectious disease (ID), and vascular access- (VA) related hospitalization rates and length of stay (LOS) were assessed. Methods: 444 prevalent diabetic dialysis patients had monthly PG, quarterly GA, and all HbA1c values recorded for 2.33 years; hospitalizations within 17 and 30 days of testing were evaluated. Best-fit, time-dependent Cox models were constructed in unadjusted, case-mix-adjusted (age, sex, race, BMI, diabetes duration, dialysis vintage), and case-mix- plus lab-adjusted (hemoglobin, albumin, phosphorus) models. Results: Mean ± SD diabetes duration was 18.5 ± 10.8 years and dialysis vintage 2.9 ± 2.6 years. In fully adjusted models, CV hospitalization rates were associated with increasing GA (HR 1.32; 95% CI 1.11–1.57; p = 0.002 at 17 days; HR 1.21; p = 0.02 at 30 days) and PG (HR 1.10; 95% CI 1.02–1.17; p = 0.01 at 17 days; HR 1.07; p = 0.03 at 30 days), not HbA1c (HR 1.24; 95% CI 0.89–1.73; p = 0.21 at 17 days; HR 1.26; p = 0.10 at 30 days). LOS for CV admissions was positively associated with GA (HR 1.18; 95% CI 1.01–1.39; p = 0.03), not PG (HR 1.04; 95% CI 0.99–1.10; p = 0.15) or HbA1c (HR 1.03; 95% CI 0.92–1.15; p = 0.21). Admissions due to ID and VA complications (and LOS) did not correlate with these assays. Conclusions: Improved glycemic control based on GA and PG predicted CV-related hospitalizations; GA also predicted CV hospitalization LOS. HbA1c did not predict cause-specific hospitalizations in dialysis populations.
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