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Abstract: SA-PO0596

Subcutaneous Adipose Tissue Immune Cell Populations and ADPKD Progression

Session Information

Category: Genetic Diseases of the Kidneys

  • 1201 Genetic Diseases of the Kidneys: Monogenic Kidney Diseases

Authors

  • Phillips, Leanna, University of Colorado Anschutz Medical Campus Department of Medicine, Aurora, Colorado, United States
  • Oh, Ester, University of Colorado Anschutz Medical Campus Department of Medicine, Aurora, Colorado, United States
  • Wang, Wei, University of Colorado Anschutz Medical Campus Department of Medicine, Aurora, Colorado, United States
  • Farmer-Bailey, Heather, University of Colorado Anschutz Medical Campus Department of Medicine, Aurora, Colorado, United States
  • Kline, Timothy L., Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Steele, Cortney, University of Colorado Anschutz Medical Campus Department of Medicine, Aurora, Colorado, United States
  • Catenacci, Victoria, University of Colorado Anschutz Medical Campus Department of Medicine, Aurora, Colorado, United States
  • Gitomer, Berenice Y., University of Colorado Anschutz Medical Campus Department of Medicine, Aurora, Colorado, United States
  • Hopp, Katharina, University of Colorado Anschutz Medical Campus Department of Medicine, Aurora, Colorado, United States
  • Chonchol, Michel, University of Colorado Anschutz Medical Campus Department of Medicine, Aurora, Colorado, United States
  • Nowak, Kristen L., University of Colorado Anschutz Medical Campus Department of Medicine, Aurora, Colorado, United States
Background

We previously reported that overweight and obesity are independent predictors of rapid kidney growth in adults with early-stage ADPKD. As obesity is associated with accumulation of pro-inflammatory immune cells in adipose tissue, such as M1-like macrophages, we hypothesized that immune cell populations in subcutaneous adipose tissue (SAT) would associate with body mass index (BMI) and height-adjusted total kidney volume (htTKV) in adults with ADPKD.

Methods

Baseline data from 30 non-diabetic adults (5M/25F) with ADPKD and BMI 25-45 kg/m2 from our ongoing clinical trial were included. Stromal vascular fractions isolated from SAT biopsies were analyzed by flow cytometry to quantify immune cell populations. Populations were compared according to BMI (overweight [BMI=25.0-29.9 kg/m2] vs. obese [BMI≥30.0 kg/m2]) and Mayo Imaging Classification (Class A/B vs. Class C/D/E) and using multivariable linear regression.

Results

Participants were age 45±11 years with a BMI of 33.2±4 kg/m2, median (IQR) htTKV of 971.0 (825.7, 1385.6) ml/m, and eGFR 73±26 ml/min/1.73m2. Surprisingly, immune cell populations were not associated with BMI. However, faster progression was associated with a lower proportion of M2-like macrophages (CD206+) as a percentage of total monocytes/macrophages (Figure). This association remained after adjusting for sex and age (β-estimate: -22.8; 95% CI: -41.9 to -3.8).

Conclusion

Faster progressing ADPKD is associated with a lower proportion of M2-like anti-inflammatory macrophages, indicating a potentially higher proportion of M1-like pro-inflammatory macrophages in SAT. Future research should evaluate if these proportions change in response to weight loss and/or attenuated kidney growth.

Funding

  • NIDDK Support

Digital Object Identifier (DOI)