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Abstract: SA-PO319

Impact of Carbamylation on the Association of Glycated Albumin and Diabetic Kidney Disease (DKD) Progression

Session Information

Category: Diabetic Kidney Disease

  • 702 Diabetic Kidney Disease: Clinical

Authors

  • Tang, Mengyao, Massachusetts General Hospital, Boston, Massachusetts, United States
  • Berg, Anders H., Cedars-Sinai Medical Center, Los Angeles, California, United States
  • Kalim, Sahir, Massachusetts General Hospital, Boston, Massachusetts, United States
Background

HbA1c is widely used to estimate glycemia, yet it is less reliable in CKD due to factors such as anemia and competition from another post-translational protein modification, carbamylation, acting on the same amino groups. We previously showed that the association between HbA1c and the risk of CKD progression was modified by anemia and carbamylation. While an alternative hemoglobin-independent glycemic marker, glycated albumin, could overcome the anemia-related limitation of HbA1c, little is known about whether it is impacted by carbamylation in CKD.

Methods

We measured baseline serum glycated albumin and carbamylated albumin levels in 1,550 patients with co-existing CKD and diabetes enrolled in the prospective Chronic Renal Insufficiency Cohort study. A Cox regression model was used to test the association between glycated albumin and CKD progression (ESKD or 50% eGFR decline), with an interaction term of glycated albumin and carbamylated albumin to evaluate whether carbamylation modified this association.

Results

Participant characteristics included mean age 60 (SD 9) years; mean eGFR 38 (15) mL/min/1.73 m2; median glycated albumin 22 (IQR 18-28) %; and median carbamylated albumin 8 (6-11) mmol/mol. Glycated albumin levels were higher in the higher carbamylated albumin quartiles. During a median 7-year follow-up, 805 (51.9%) individuals developed CKD progression. Overall, higher glycated albumin levels (restricted cubic spline or quartiles) were independently associated with greater risks of CKD progression (Fig 1): compared with quartile 1, those in quartile 4 had a 1.35-fold greater risk (95% CI, 1.10 to 1.66). Interaction testing between glycated albumin and carbamylated albumin was not significant (P = 0.43).

Conclusion

In patients with CKD and diabetes, the association between glycated albumin and CKD progression is not modified by carbamylation. This finding suggests that glycated albumin could overcome the carbamylation-related limitation of HbA1c in CKD.

Fig 1. Adjusted HR for Glycated Albumin and Risks of CKD Progression

Funding

  • NIDDK Support