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Abstract: FR-PO732

Urinary CD206+ Cells Correlate with Rate of Renal Function Loss in Autosomal Dominant Polycystic Kidney Disease

Session Information

Category: Genetic Diseases of the Kidneys

  • 1001 Genetic Diseases of the Kidneys: Cystic

Authors

  • Li, Zhang, University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Zimmerman, Kurt, University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Chacana, Teresa, University of Alabama at Birmingham, Birmingham, Alabama, United States
  • George, James F., University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Yoder, Bradley K., University of Alabama at Birmingham, Birmingham, Alabama, United States
  • Mrug, Michal, University of Alabama at Birmingham, Birmingham, Alabama, United States
Background

We showed that tissue-resident macrophages promote renal cystic disease severity in mice; however, the relevance of this observation to ADPKD patients was unknown. While key markers that define these resident macrophages in mice cannot be used in humans (e.g., mouse marker F4/80 is encoded by gene Emr1; it is expressed exclusively by human eosinophils), we recently identified CD206 as a candidate marker of human resident macrophages.

Methods

We evaluated CD206+ immune cell populations in kidneys from ADPKD patients (vs non-ADPKD controls) using flow cytometry and confocal immunofluorescence microscopy approaches. We used similar analyses for analyses of CD206+ cells in urine samples from ADPKD patients.

Results

We found that CD206+ cells accumulated in regions adjacent to renal cysts. While the average number of intrarenal CD206 cells was higher in ADPKD kidneys (vs controls), the variability was high and this difference did not reach statistical significance (0.0252 vs. 0.006 percent of total renal cells; p =0.170). Also, we found that the urinary CD206+ cell-based index (e.g., after adjustment for urine creatinine concentration) correlated moderately with a rate of GFR decline (over 5 years) in a small cohort of ADPKD patients (n=30). This effect was independent of kidney length (KL), recently described CKD stage 3B predictor in ADPKD with similar AUC 0.88 as height-adjusted total kidney volume. The correlation between average GFR decline rates and KL was comparably strong (r=0.400; p=0.029), the correlation between the eGFR decline rates and urine albumin to creatinine ratio was weaker (ACR; r=0.192) in this cohort.

Conclusion

Together with studies on resident macrophages in animal models, these data suggest that resident renal macrophages participate in the disease pathogenesis in ADPKD patients. They also point to urinary CD206+ cells as a novel candidate marker of the disease activity in ADPKD.

Funding

  • NIDDK Support