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Kidney Week

Abstract: FR-OR05

Kidney-Adipose Tissue Cross-Talk during Weight Loss in Adults with Obesity and CKD

Session Information

Category: CKD (Non-Dialysis)

  • 2302 CKD (Non-Dialysis): Clinical, Outcomes, and Trials

Authors

  • MacLaughlin, Helen L., Queensland University of Technology, Brisbane, Queensland, Australia
  • Yuen, Ying Chun, Queensland University of Technology, Brisbane, Queensland, Australia
  • Conley, Marguerite M., Queensland University of Technology, Brisbane, Queensland, Australia
  • Philp, Lisa K., Queensland University of Technology, Brisbane, Queensland, Australia
Background

Mechanisms linking obesity and chronic kidney disease (CKD) include energy, adipokine and metabolic homeostasis imbalances. Adiponectin, leptin and fetuin-A play critical roles in these pathophysiological processes, contributing to insulin resistance, inflammation and kidney damage. This study investigated the effect of intentional weight loss on adipokines, fetuin-A, and urinary NGAL levels in people living with obesity and CKD.

Methods

Blood and urine samples were obtained at baseline, 3 and 6 months from 49 adults with BMI >30kg/m2, CKD stages 1-3b and urinary protein/creatinine ratio >3mg/mmol, who were randomised to either a low energy diet and exercise intervention (LED) or usual care (UC) in the SLOW CKD feasibility study. Serum adiponectin, leptin, fetuin-A, cystatin-C and urinary NGAL levels were measured using commercially available quantitative sandwich enzyme-linked immunosorbent assays (ELISA). Median differences using Mann-Whitney tests and associations between changes in variables using linear or rank regression were examined.

Results

Median BMI, estimated glomerular filtration rate (eGFR) and urinary protein to creatinine ratio were 38.6 kg/m2, 57 mL/min/1.73m2 and 84 mg/mmol respectively at baseline. Median weight change was -9 kg (IQR -12 to -7) in LED and 0.5 kg (IQR -4 to 2) in UC at 6M. Biomarker data were available for 35 participants (14 LED, 21 UC). Leptin was high (41.2 ± 27.7 ng/mL), and adiponectin was low (12.6 ± 16.1 μg/mL) at baseline across groups. Adiponectin/leptin ratio improved in LED and remained unchanged in UC (p=0.45), and was inversely associated with weight loss (r=-0.49, p=0.008) and trended towards positive association with fetuin-A (r=0.42 p=0.08) at 6M. Change in leptin was associated with weight (r=0.71, p〈0.001) and waist circumference (r=0.57, p=0.001) changes at 6M. Change in fetuin-A was inversely associated with change in cystatin-C at 6M (r=-0.59, p=0.008). Urinary NGAL was unexpectedly inversely associated with weight loss at 6M (r=-0.43, p=0.02).

Conclusion

Adults with obesity and CKD had altered leptin and adiponectin levels, and intentional weight loss resulted in favourable changes in adiponectin/leptin ratio and fetuin-A, which was associated with reduced cystatin-C. Findings demonstrate potential kidney-adipose tissue cross-talk mechanisms linking obesity and CKD.

Funding

  • Private Foundation Support