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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

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posted on 2020-10-06, 19:34 authored by Yang Xu, Aditya Surapaneni, Jim Alkas, Marie Evans, Jung-Im Shin, Elizabeth Selvin, Alex Chang, Morgan E Grams, Juan Jesus Carrero
Objective: 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.

Research Design and Methods: In two observational cohorts of U.S. (Geisinger Heath system, Pennsylvania) and Swedish (SCREAM project, Stockholm) adults with type-2 diabetes and confirmed CKD stages G3-G5 undergoing routine care, we evaluated associations between baseline and time-varying HbA1c with the incident AKI (defined as increase in creatinine ≥0.3 mg/dL over 48 hours, 1.5x creatinine over 7 days).

Results: In the U.S. cohort, there were 22877 patients (55% women) with median age 72 years and eGFR 52 ml/min/1.73 m2. In the Swedish cohort, there were 12157 patients (51% women) with median age 76 years and eGFR 51 ml/min/1.73 m2. During 3.1 and 2.3 years of follow-up, 7060 and 2619 AKI events were recorded in the U.S. and Swedish cohorts, respectively. The adjusted association between baseline HbA1c and AKI was similar in both cohorts. Compared to baseline HbA1c 6-6.9% (42-52 mmol/mol), the HR for AKI in patients with HbA1c>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 HbA1c.

Conclusions: Higher HbA1c was associated with AKI in adults with type 2 diabetes and CKD, suggesting that improving glycemic control may reduce the risk of AKI.


Research reported in this publication was supported by the Swedish Research Council 2019-01059 (PI: Dr. Carrero), R01 DK115534 and R01 DK100446 (PI: Dr Grams), and K01 DK121825 (PI: Dr. Shin) from the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. The funding sources had no role in the design and conduct of the study, analysis or interpretation of the data, and preparation or final approval of the manuscript before publication.


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