Dataset Information

Associations of Glycated Albumin and HbA1c with Chronic Kidney Disease in US Adults.

ABSTRACT:

Background

Glycated albumin may provide complementary information to hemoglobin A1c (HbA1c). We compared cross-sectional associations of HbA1c and glycated albumin with chronic kidney disease (CKD) in US adults.

Methods

We included 10 923 adults (9955 without diagnosed diabetes, 968 with a diabetes diagnosis) from the National Health and Nutrition Examination Survey 1999-2004. We examined continuous associations and clinical cut points for HbA1c among those without diabetes (<5.0%, 5.0%-5.6% (reference), 5.7%-6.4%, ≥6.5%) and among those with diagnosed diabetes (<7.0%, 7.0%-8.9%, ≥9.0%) and percentile equivalents for glycated albumin. We used logistic regression to compare associations with prevalent CKD, adjusting for traditional risk factors. We used likelihood ratio tests to assess whether adding glycated albumin improved the model with HbA1c.

Results

There were J-shaped associations for both glycated albumin and HbA1c with CKD. Persons without a history of diabetes and very low glycated albumin or HbA1c were more likely to have CKD compared to those without diabetes and normoglycemia. The odds ratios (ORs) for CKD were 1.32 (95% CI, 1.12-1.55) for HbA1c 5.7% to 6.4% and 2.04 (95% CI, 1.28-3.25) for HbA1c ≥6.5%. The ORs for glycated albumin were 1.27 (95% CI, 1.06-1.51) and 2.48 (95% CI, 1.50-4.08) for glycated albumin 14.4% to 17.8% and ≥17.9%, respectively. The inclusion of glycated albumin in the model with HbA1c and traditional risk factors modestly but significantly improved the model fit (P value = 0.006).

Conclusions

Glycated albumin and HbA1c were similarly associated with prevalent CKD. Glycated albumin provides complementary information to HbA1c for prevalent CKD.

SUBMITTER: Kim H

PROVIDER: S-EPMC9246894 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Glycated albumin (GA) exhibits atherogenic effects and increased serum GA levels are associated with the development of cardiovascular complications in diabetic patients. GA production also increases with aging, oxidative stress, and renal dysfunction. We performed this study to further ascertain the association between GA and arterial stiffness in nondiabetic chronic kidney disease (CKD) patients. We enrolled 129 nondiabetic CKD patients. Arterial stiffness was measured by brachial-ankle pulse wave velocity (baPWV) using a volume plethysmographic instrument along with simultaneous measurements of GA. Insulin resistance was determined with the homeostatic model assessment. The estimated glomerular filtration rate was calculated using serum creatinine and cystatin C according to the CKD-EPI Creatinine-Cystatin C equation adjusted for age, sex, and race (eGFRcr-cys). Nondiabetic CKD patients with arterial stiffness (baPWV ?1400?cm/s) showed higher GA levels than those without arterial stiffness (14.2 [8.7-20.2]% vs 13.0 [8.8-18.9]%, P?=?0.004). In the subgroup analysis, the patients who had both a higher GA level and a lower eGFRcr-cys, showed the highest baPWV compared with patients with a higher GA or a lower GFR alone. By Spearman's correlation analysis, GA correlated significantly with baPWV (r?=?+0.291, P?=?0.001) and fasting serum glucose level (r?=?+0.191, P?=?0.030), whereas The homeostatic model assessment of insulin resistance did not show any significant correlation with baPWV. Systolic blood pressure (r?=?+0.401 P?<?0.001), age (r?=?+0.574, P?<?0.001), high-density lipoprotein (HDL)-cholesterol level (r?=?-0.317, P?<?0.001), and eGFRcr-cys (r?=?-0.285, P?=?0.002) had a significant correlation with baPWV. According to multivariable logistic regression analysis, higher GA and systolic blood pressure were the independent risk factors affecting arterial stiffness. Our results suggest that serum GA is a potential risk factor of arterial stiffness in nondiabetic CKD patients.