Petter Bjornstad1, Laura Pyle2, Gregory L Kinney3, Marian Rewers4, Richard J Johnson5, David M Maahs6, Janet K Snell-Bergeon4. 1. Department of Pediatric Endocrinology, University of Colorado School of Medicine, Aurora, CO, United States; Barbara Davis Center for Diabetes, University of Colorado School of Medicine, Aurora, CO, United States. Electronic address: Petter.Bjornstad@childrenscolorado.org. 2. Department of Pediatric Endocrinology, University of Colorado School of Medicine, Aurora, CO, United States; Department of Biostatistics and Informatics, Colorado School of Public Health, Aurora, CO. 3. Barbara Davis Center for Diabetes, University of Colorado School of Medicine, Aurora, CO, United States; Department of Epidemiology, Colorado School of Public Health, Aurora, CO. 4. Department of Pediatric Endocrinology, University of Colorado School of Medicine, Aurora, CO, United States; Barbara Davis Center for Diabetes, University of Colorado School of Medicine, Aurora, CO, United States. 5. Department of Medicine, Division of Nephrology, University of Colorado School of Medicine, Aurora, CO, United States. 6. Department of Pediatric Endocrinology, University of Colorado School of Medicine, Aurora, CO, United States; Barbara Davis Center for Diabetes, University of Colorado School of Medicine, Aurora, CO, United States; Department of Medicine, Division of Nephrology, University of Colorado School of Medicine, Aurora, CO, United States.
Abstract
OBJECTIVE: The associations between elevated adiponectin and end-stage renal disease are well recognized and thought to be at least partially explained by reduced renal clearance. Conversely, the relationship between adiponectin and early diabetic kidney disease (DKD) with preserved glomerular filtration rate (GFR), including rapid GFR decline and incident chronic kidney disease (CKD) is unclear. We hypothesized that elevated adiponectin would be associated with early DKD in adults with type 1 diabetes. METHODS: Adults with type 1 diabetes (n=646 at baseline, n=525 at 6years) had adiponectin and renal function by estimated GFR (eGFR) by CKD-EPI creatinine and albumin-excretion rate (AER) evaluated at baseline and 6years. Linear and logistic models evaluated the associations of baseline adiponectin with AER, macroalbuminuria (AER ≥200μg/min), eGFR, CKD (<60mL/min/1.73m2) and rapid GFR decline (>3mL/min/1.73m2/year). Models adjusted for age, sex, duration, HbA1c, SBP, LDL-C and current smoking. RESULTS: Compared to non-diabetics, adults with type 1 diabetes had significantly higher adiponectin, and the difference remained significant after adjusting for AER and/or eGFR (p<0.0001). Adiponectin at baseline was positively associated with rapid GFR decline (OR: 1.24, 95% CI 1.00-1.53), incident CKD (OR: 1.75, 1.14-2.70), and persistent macroalbuminuria and CKD (OR: 1.61, 1.10-2.36) over 6years in adjusted models. The associations also remained significant after further adjustments for CRP, estimated insulin sensitivity and ACEi/ARB therapy. CONCLUSIONS: Adults with type 1 diabetes have higher adiponectin than their non-diabetic peers, and elevated adiponectin at baseline is independently associated with greater odds of developing early DKD over 6years.
OBJECTIVE: The associations between elevated adiponectin and end-stage renal disease are well recognized and thought to be at least partially explained by reduced renal clearance. Conversely, the relationship between adiponectin and early diabetic kidney disease (DKD) with preserved glomerular filtration rate (GFR), including rapid GFR decline and incident chronic kidney disease (CKD) is unclear. We hypothesized that elevated adiponectin would be associated with early DKD in adults with type 1 diabetes. METHODS: Adults with type 1 diabetes (n=646 at baseline, n=525 at 6years) had adiponectin and renal function by estimated GFR (eGFR) by CKD-EPI creatinine and albumin-excretion rate (AER) evaluated at baseline and 6years. Linear and logistic models evaluated the associations of baseline adiponectin with AER, macroalbuminuria (AER ≥200μg/min), eGFR, CKD (<60mL/min/1.73m2) and rapid GFR decline (>3mL/min/1.73m2/year). Models adjusted for age, sex, duration, HbA1c, SBP, LDL-C and current smoking. RESULTS: Compared to non-diabetics, adults with type 1 diabetes had significantly higher adiponectin, and the difference remained significant after adjusting for AER and/or eGFR (p<0.0001). Adiponectin at baseline was positively associated with rapid GFR decline (OR: 1.24, 95% CI 1.00-1.53), incident CKD (OR: 1.75, 1.14-2.70), and persistent macroalbuminuria and CKD (OR: 1.61, 1.10-2.36) over 6years in adjusted models. The associations also remained significant after further adjustments for CRP, estimated insulin sensitivity and ACEi/ARB therapy. CONCLUSIONS: Adults with type 1 diabetes have higher adiponectin than their non-diabetic peers, and elevated adiponectin at baseline is independently associated with greater odds of developing early DKD over 6years.
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