Glycemic Control and the Risk of Acute Kidney Injury in Patients With Type 2 Diabetes and Chronic Kidney Disease: Parallel Population-Based Cohort Studies in U.S. and Swedish Routine Care.

Abstract

Patients with diabetes and chronic kidney disease (CKD) have increased susceptibility to acute kidney injury (AKI), but mechanisms are unclear. We investigated the association of glycemic control with risk of AKI. In two observational cohorts of U.S. (Geisinger Health System, Danville, PA) and Swedish (Stockholm CREAtinine Measurements [SCREAM] project, Stockholm, Sweden) adults with type 2 diabetes and confirmed CKD stages G3-G5 undergoing routine care, we evaluated associations between baseline and time-varying hemoglobin A_1c (HbA_1c) with the incident AKI (defined as increase in creatinine ≥0.3 mg/dL over 48 h or 1.5 times creatinine over 7 days). In the U.S. cohort, there were 22,877 patients (55% women) with a median age of 72 years and estimated glomerular filtration rate (eGFR) 52 mL/min/1.73 m². In the Swedish cohort, there were 12,157 patients (50% women) with a median age of 77 years and eGFR 51 mL/min/1.73 m². During 3.1 and 2.3 years of follow-up, 7,060 and 2,619 AKI events were recorded in the U.S. and Swedish cohorts, respectively. The adjusted association between baseline HbA_1c and AKI was similar in both cohorts. Compared with baseline HbA_1c 6-6.9% (42-52 mmol/mol), the hazard ratio for AKI in patients with HbA_1c >9% (75 mmol/mol) was 1.29 (95% CI 1.18-1.41) in Geisinger and 1.33 (95% CI 1.13-1.57) in the Swedish cohort. Results were consistent in stratified analysis, when using death as competing risk, and when using time-varying HbA_1c. Higher HbA_1c was associated with AKI in adults with type 2 diabetes and CKD, suggesting that improving glycemic control may reduce the risk of AKI.