The Effect of Surgical Weight Loss on Diabetic Complications in the Severely Obese

The aim of this study was to determine the effect of surgical weight loss on chronic kidney disease (CKD) , retinopathy, and cardiovascular autonomic neuropathy (CAN) in people with severe obesity. We completed a prospective cohort study of participants with severe obesity who underwent bariatric surgery. At baseline and at 2 years following bariatric surgery, participants had outcome measurements and underwent metabolic phenotyping. The updated National Cholesterol Education Program (NCEP) criteria were used to define the metabolic syndrome (MetS) and its individual components. The primary outcome for CKD was the estimated Glomerular Filtration Rate (eGFR) , retinopathy was mean deviation on frequency doubling technology testing, and CAN was the expiration/inspiration (E/I) ratio. Among 138 baseline participants, 80 (mean (standard deviation) age: 45.6 (11.2) years, 72.5% female) completed 2 years of follow-up. Participants lost 31.9 (17.5) kg. All metabolic syndrome components improved with the exception of blood pressure. CKD worsened (eGFR: baseline: 85.6 (19.7) , 2-year: 82.6 (23.1) , p=0.04) , retinopathy was stable (mean deviation: baseline: −1.2 (4.3) , 2-year: −1.6 (4.2) , p=0.53) , and CAN was stable (E/I ratio: baseline: 1.18 (0.12) , 2-year: 1.18 (0.11) , p=0.95) following bariatric surgery. Greater reduction in fasting glucose was associated with significant improvements to primary CKD (eGFR: point estimate (PE) : -0.22, 95% Confidence Interval (CI) : −0.38, −0.06) and retinopathy (mean deviation: PE: -0.04, 95%CI: −0.08, −0.004) , after adjusting for age, sex, and baseline BMI. Surgical weight loss was associated with improvements in all metabolic parameters except blood pressure. Despite the improvement to metabolic risk factors, CKD significantly worsened during follow-up, whereas retinopathy and CAN outcomes remained stable. This stability may be an improvement compared to the natural progression of these conditions, however controlled trials are needed to confirm. Disclosure E.L.Reynolds: None. M.Watanabe: None. M.Elafros: None. E.L.Feldman: None. B.C.Callaghan: None. Funding The project described was supported by Grant Number P30DK020572 (MDRC) from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) . Dr. Callaghan is currently funded by a NIH NIDDK R-award (DK115687) . Dr. Reynolds was supported by NIH T32 (NS0007222) . Dr. Feldman was supported by an NIH NIDDK DP3 award (DK094292) and is currently funded by NIH NIDDK (R24082841 and R21 NS102924) and the Novo Nordisk Foundation Center for Basic Metabolic Research (NNF14°C0011633) . Dr. Reynolds, Dr. Callaghan, and Dr. Feldman receive support from the NeuroNetwork for Emerging Therapies and the A. Alfred Taubman Research Institute at the University of Michigan.