Abstract: PO2529
Obesity and Poorer Renal Allograft Function: Analysis of Longitudinal Data
Session Information
- Transplant Complications: Cardiovascular, Metabolic, and Societal
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 1902 Transplantation: Clinical
Authors
- Tantisattamo, Ekamol, Division of Nephrology, Hypertension and Kidney Transplantation, Department of Medicine, University of California Irvine School of Medicine, Orange, California, United States
- Songtanin, Busara, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand
- Leelaviwat, Natnicha, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand
- Saowapa, Sakditad, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand
- Vutthikraivit, Possawat, Phramongkutklao College of Medicine, Mahidol University,, Bangkok, Thailand
- Lopimpisuth, Chawit, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand
- Polpichai, Natchaya, Faculty of Medicine Songklanagarin Hospital, Prince of Songkla University, Songkla, Thailand
Background
Obesity is associated with worsened allograft function, but its effect on allograft function after established baseline allograft function at a 12-week post kidney transplant (KT) is unclear.
Methods
All 105 KT recipients were divided into obese (BMI ≥30 kg/m2) and non-obese groups. Longitudinal data were analyzed by linear mixed model to examine association between obesity and eGFR during the 1st year post-KT.
Results
Mean age was 54±11 years and 64 patients (61%) was female. Seventy-one patients (68%) were obese. Generalized estimating equation revealed that eGFR increased 0.16 ml/min/1.73 m2 (β±SE 0.16±0.04; 95%CI 0.09 to 0.23) for every 1 week after KT. Excluding eGFR at 4-week post-KT when baseline allograft function is generally not established, mean eGFR at 12-week post-KT was the lowest and assigned as the baseline allograft function. Given unequal spreading of time when eGFR were measured, a 1-year follow-up was categorized into every 4 and 12 weeks if eGFR were measured before and after a 12-week post-KT, respectively. Spline interaction term was created at the 12-week post-KT as well as categorized time-spline interaction term. By using a linear mixed model and after adjusted for age, gender, type of KT (deceased vs living donor KT), obesity category and its interaction team with categorized time and spline interaction term, obese group had a higher rate of eGFR decline of 2.9 ml/min/1.73 m2 every 4 weeks prior to 12-week post-KT, and the rate declined to 1.1 ml/min/1.73 m2 every 12 weeks after 12-week post-KT. At the 12-week post when baseline eGFR was established, eGFR were 74.1±30.5 and 78.0±30.5 ml/min/1.73 m2 for obese and non-obese groups, respectively (random intercept); whereas, rate of increase in eGFR of those corresponding groups were 69.3±0.2 and 70.3±0.2 ml/min/1.73 m2 every 12 weeks (random slope).
Conclusion
Although population-based estimated eGFR was significantly increased overtime, obese KT recipients had lower baseline eGFR at the 12-week post-KT and slower rate of increased eGFR than those of non-obese group when individual baseline eGFR at the 12-week post-KT and rate of eGFR change were taken into the consideration. Pre-KT obesity remains one of the associated factors of poor allograft outcomes, which may be mitigated by pre-KT weight loss.