Anna R Kahkoska1, Scott Isom2, Jasmin Divers2, Elizabeth J Mayer-Davis3, Lawrence Dolan4, Amy S Shah4, Maryam Afkarian5, David J Pettitt6, Jean M Lawrence7, Santica Marcovina8, Sharon H Saydah9, Dana Dabelea10, David M Maahs11, Amy K Mottl12. 1. Department of Nutrition, University of North Carolina at Chapel Hill, 135 Dauer Drive, Chapel Hill, NC 27599, USA. Electronic address: anna_kahkoska@med.unc.edu. 2. Dept. of Biostatistical Sciences, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA. 3. Department of Medicine, University of North Carolina at Chapel Hill, 321 S. Columbia St, Chapel Hill, NC 27516, USA. 4. Division of Endocrinology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Ave, Cincinnati, OH 45229, USA. 5. Division of Nephrology, Department of Medicine, University of California, Davis, 4610 X St, Sacramento, CA 95817, USA. 6. 2219 Bath St., Santa Barbara, CA 93105, USA. 7. Department of Research & Evaluation, Kaiser Permanente Southern California, 100 S Los Robles Ave, Pasadena, CA 91101, USA. 8. Northwest Lipid Metabolism and Diabetes Research Laboratories, Dept. of Medicine, University of Washington, 401 Queen Anne Avenue North, UW Mailbox 359119, Seattle, WA 98109, USA. 9. Division of Diabetes Translation, US Centers for Disease Control and Prevention, National Center for Health Statistics, 3311 Toledo Rd, Hyattsville, MD 20782, USA. 10. Department of Epidemiology, School of Public Health, University of Colorado Denver, 13001 E 17th Pl, Aurora, CO 80045, USA. 11. Division of Pediatric Endocrinology, Stanford University School of Medicine, 291 Campus Drive, Stanford, CA 94305, USA. 12. University of North Carolina Kidney Center, UNC School of Medicine, 101 Manning Dr, Chapel Hill, NC 27514, USA.
Abstract
AIMS: To determine among adolescents and young adults with youth-onset type 1 diabetes and type 2 diabetes the rates and risk factors for albuminuria regression and progression. METHODS: Data from SEARCH, a longitudinal observational study of youth-onset type 1 diabetes (N = 1316) and type 2 diabetes (N = 143) were analyzed. Urine albumin:creatinine ratio (UACR) was measured from random urine specimens at baseline and follow-up visits (mean 7 years later). Albuminuria regression was defined as halving of baseline UACR when baseline UACR was ≥30 μg/mg; progression was defined as doubling of baseline UACR when follow-up UACR was ≥30 μg/mg, respectively. Multivariable regression assessed risk factors associated with low-risk albuminuria category (combined persistently-low albuminuria and regression) versus moderate-risk albuminuria category (combined persistently-high albuminuria and progression). RESULTS: Albuminuria progression was more common in type 2 diabetes versus type 1 diabetes (15.4% versus 6.0%, p<0.001). Moderate-risk albuminuria was associated with increasing HbA1c (adjusted OR (aOR) = 1.3, 95% CI 1.1-1.6) and lack of private health insurance (aOR = 2.7, 95%CI 1.1-6.5) in type 1 diabetes; and African American race (OR = 4.6, 95% CI 1.2-14.2), lower estimated insulin sensitivity score (aOR = 2.1, 95% CI 1.4-3.3), baseline UACR (aOR = 3.2, 95% CI 1.7-5.8), and follow-up estimated glomerular filtration rate (eGFR) (10-unit increase aOR = 1.3, 95% CI 1.0, 1.5) in type 2 diabetes. CONCLUSIONS: In the first decade of diabetes duration, kidney complications in type 2 diabetes are significantly more aggressive than in type 1 diabetes and may be associated with less modifiable risk factors including race, insulin sensitivity, and eGFR. Early interventions may help reduce long-term kidney complications.
AIMS: To determine among adolescents and young adults with youth-onset type 1 diabetes and type 2 diabetes the rates and risk factors for albuminuria regression and progression. METHODS: Data from SEARCH, a longitudinal observational study of youth-onset type 1 diabetes (N = 1316) and type 2 diabetes (N = 143) were analyzed. Urine albumin:creatinine ratio (UACR) was measured from random urine specimens at baseline and follow-up visits (mean 7 years later). Albuminuria regression was defined as halving of baseline UACR when baseline UACR was ≥30 μg/mg; progression was defined as doubling of baseline UACR when follow-up UACR was ≥30 μg/mg, respectively. Multivariable regression assessed risk factors associated with low-risk albuminuria category (combined persistently-low albuminuria and regression) versus moderate-risk albuminuria category (combined persistently-high albuminuria and progression). RESULTS: Albuminuria progression was more common in type 2 diabetes versus type 1 diabetes (15.4% versus 6.0%, p<0.001). Moderate-risk albuminuria was associated with increasing HbA1c (adjusted OR (aOR) = 1.3, 95% CI 1.1-1.6) and lack of private health insurance (aOR = 2.7, 95%CI 1.1-6.5) in type 1 diabetes; and African American race (OR = 4.6, 95% CI 1.2-14.2), lower estimated insulin sensitivity score (aOR = 2.1, 95% CI 1.4-3.3), baseline UACR (aOR = 3.2, 95% CI 1.7-5.8), and follow-up estimated glomerular filtration rate (eGFR) (10-unit increase aOR = 1.3, 95% CI 1.0, 1.5) in type 2 diabetes. CONCLUSIONS: In the first decade of diabetes duration, kidney complications in type 2 diabetes are significantly more aggressive than in type 1 diabetes and may be associated with less modifiable risk factors including race, insulin sensitivity, and eGFR. Early interventions may help reduce long-term kidney complications.
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