Author + information
- Şükrü Akyüz1,
- Selçuk Yazıcı1,
- Barış Yaylak2,
- Barış Güngör1,
- Kıvılcım Özden1,
- Tuğba Kemaloğlu Öz1,
- Servet Altay1,
- Mehmet Karaca1,
- Güney Erdoğan3,
- Zekeriya Nurkalem1 and
- Hülya Kaşıkçıoğlu1
Type 2 diabetes mellitus (T2DM) is known as a major risk factor for developing contrast-induced acute kidney injury (CI-AKI). However, it is not clear whether relatively chronic elevation of blood glucose level, or elevated glycosylated hemoglobin A1c (HbA1c) is associated with the incidence of CI-AKI.
The present study prospectively enrolled 133 patientswith T2DM undergoing elective coronary angiography and/or intervention with a non-ionic low-osmolality contrast media (CM). The patients were divided into two groups: those with an HbA1c of <6.5% and those with an HbA1c of ≥6.5%. All patients had similar baseline characteristics and were hydrated appropriately. Iftaking metformin, it was continued because of the low risk of developing lactic acidosis in patients with an estimated glomerular filtration rate of ≥60 mL/min/1.73 m2, as in this cohort. When necessary, insulin was administered to optimize glucose level in the peri-procedural period. The outcome was assessed by the occurrence of CI-AKI.
CI-AKI which was defined as ≥25% relative increase in serum creatinine from the baseline at 48 hours after administration of CM, occurred in 1/24 patients (4.1%) with optimal HbA1c levels (<6.5%), and 6/109 (5.5%) patients with high HbA1c levels (≥6.5%), (p=0.79). When the cut-offpoint of HbA1c was chosen as 7%, again there was no statistically significant difference between the two groups [2/41 (4.9%) vs. 5/92 (5.4%), p=0.89]. When different CI-AKI definitions were taken into account, there was also no statistically significant difference between the two groups despite a high variability in the incidence of CI-AKI.
Elevated HbA1c is not associated with the incidence of CI-AKI in patients with T2DM undergoing coronary angiography and/or intervention.
|HbA1c <6.5 (N=24)||HbA1c ≥6.5 (N=109)||p|
|Pre-procedure SCr (IQR), mg/dL||0.90 (0.20)||0.90 (0.25)||0.57|
|Pre-procedure eGFR (IQR), mL/min/1.73 m2||82.1 (31.0)||89.4 (33.1)||0.40|
|Total volume of hydration, mL||2923±1290||3165±1070||0.29|
|Amount of the contrast media (IQR), mL||80 (80)||80 (68)||0.39|
CI-AKI indicates contrast-induced acute kidney injury; IQR, interquartile range; SCr, serum creatinine; eGFR, estimated glomerular filtration rate
(N=24), n (%)
(N=109), n (%)
(N=41), n (%)
(N=92), n (%)
|SCr increase by ≥25%||1 (4.1)||6 (5.5)||0.79||2 (4.9)||5 (5.4)||0.89|
|SCr increase by 0.5 mg/dL||0||4 (3.7)||0.34||1 (2.4)||3 (3.2)||0.79|
|SCr increase by ≥50%||0||3 (2.8)||0.41||1 (2.4)||2 (2.2)||0.92|
|SCr increase by 0.3 mg/dL||1 (4.1)||6 (5.5)||0.79||2 (4.9)||5 (5.4)||0.89|
|eGFR decrease by ≥25%||4 (16.7)||12 (11.0)||0.44||5 (12.2)||11 (11.9)||0.97|
CI-AKI indicates contrast-induced acute kidney injury; SCr, serum creatinine; eGFR, estimated glomerular filtration rate