Katherine D Westreich1, Scott Isom2, Jasmin Divers3, Ralph D'Agostino4, Jean M Lawrence5, Roopa Kanakatti Shankar6, Lawrence M Dolan7, Giuseppina Imperatore8, Dana Dabelea9, Elizabeth J Mayer-Davis10, Amy K Mottl11. 1. University of North Carolina Kidney Center, UNC School of Medicine, Chapel Hill, NC, United States of America. Electronic address: kdwestre@email.unc.edu. 2. Department of Biostatistical Sciences, Wake Forest University School of Medicine, Winston-Salem, NC, United States of America. Electronic address: sisom@wakehealth.edu. 3. Department of Biostatistical Sciences, Wake Forest University School of Medicine, Winston-Salem, NC, United States of America. Electronic address: jasmin.divers@nyulangone.org. 4. Department of Biostatistical Sciences, Wake Forest University School of Medicine, Winston-Salem, NC, United States of America. Electronic address: rdagosti@wakehealth.edu. 5. Department of Research and Evaluation, Kaiser Permanente Southern California, Pasadena, CA, United States of America. Electronic address: Jean.M.Lawrence@kp.org. 6. Division of Endocrinology, Children's National Medical Center, Washington, DC, United States of America. 7. Division of Endocrinology, Cincinnati Children's Hospital, Cincinnati, OH, United States of America. Electronic address: Larry.Dolan@cchmc.org. 8. Division of Diabetes Translation, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, GA, United States of America. Electronic address: gai5@cdc.org. 9. Department of Epidemiology, School of Public Health, University of Colorado Denver, Aurora, CO, United States of America. Electronic address: Dana.Dabelea@cuanschutz.edu. 10. Department of Nutrition, University of North Carolina Gillings School of Global Public Health, Chapel Hill, NC, United States of America; Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, NC, United States of America. Electronic address: mayerdav@email.unc.edu. 11. University of North Carolina Kidney Center, UNC School of Medicine, Chapel Hill, NC, United States of America. Electronic address: amy_mottl@med.unc.edu.
Abstract
AIMS: We sought to characterize the direction and associated factors of eGFR change following diagnosis of youth-onset type 1 and type 2 diabetes. METHODS: We assessed the direction of eGFR change at two visits (mean 6.6 years apart) in SEARCH, a longitudinal cohort study of youth-onset type 1 and type 2 diabetes. We used the CKiDCr-CysC equation to estimate GFR and categorized 'rising' and 'declining' eGFR as an annual change of ≥3 ml/min/1.73 m2 in either direction. Multivariable logistic regression evaluated factors associated with directional change in eGFR. RESULTS: Estimated GFR declined in 23.8% and rose in 2.8% of participants with type 1 diabetes (N = 1225; baseline age 11.4 years), and declined in 18.1% and rose in 15.6% of participants with type 2 diabetes (N = 160; baseline age 15.0 years). Factors associated with rising and declining eGFR (versus stable) in both type 1 and type 2 diabetes included sex, age at diagnosis, baseline eGFR and difference in fasting glucose between study visits. Additional factors in type 1 diabetes included time from baseline visit, HbA1c and body mass index. CONCLUSIONS: Over the first decade of diabetes, eGFR decline is more common in type 1 diabetes whereas eGFR rise is more common in type 2 diabetes.
AIMS: We sought to characterize the direction and associated factors of eGFR change following diagnosis of youth-onset type 1 and type 2 diabetes. METHODS: We assessed the direction of eGFR change at two visits (mean 6.6 years apart) in SEARCH, a longitudinal cohort study of youth-onset type 1 and type 2 diabetes. We used the CKiDCr-CysC equation to estimate GFR and categorized 'rising' and 'declining' eGFR as an annual change of ≥3 ml/min/1.73 m2 in either direction. Multivariable logistic regression evaluated factors associated with directional change in eGFR. RESULTS: Estimated GFR declined in 23.8% and rose in 2.8% of participants with type 1 diabetes (N = 1225; baseline age 11.4 years), and declined in 18.1% and rose in 15.6% of participants with type 2 diabetes (N = 160; baseline age 15.0 years). Factors associated with rising and declining eGFR (versus stable) in both type 1 and type 2 diabetes included sex, age at diagnosis, baseline eGFR and difference in fasting glucose between study visits. Additional factors in type 1 diabetes included time from baseline visit, HbA1c and body mass index. CONCLUSIONS: Over the first decade of diabetes, eGFR decline is more common in type 1 diabetes whereas eGFR rise is more common in type 2 diabetes.
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