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Abstract: SA-PO319

Hemodialysis-Associated Increase in Plasma Glial Fibrillary Acidic Protein, an Acute Brain Injury Biomarker

Session Information

Category: Dialysis

  • 701 Dialysis: Hemodialysis and Frequent Dialysis

Authors

  • Wang, Lin-Chun, Renal Research Institute, New York, New York, United States
  • Thwin, Ohnmar, Renal Research Institute, New York, New York, United States
  • Patel, Amrish U., Renal Research Institute, New York, New York, United States
  • Zhang, Hanjie, Renal Research Institute, New York, New York, United States
  • Debure, Ludovic, NYU Langone Health, New York, New York, United States
  • Wang, Xin, Renal Research Institute, New York, New York, United States
  • Grobe, Nadja, Renal Research Institute, New York, New York, United States
  • Tao, Xia, Renal Research Institute, New York, New York, United States
  • Thijssen, Stephan, Renal Research Institute, New York, New York, United States
  • Wisniewski, Thomas, NYU Langone Health, New York, New York, United States
  • Kotanko, Peter, Renal Research Institute, New York, New York, United States
Background

Structural and functional brain pathologies (e.g., cerebral hypoperfusion, silent cerebral infarcts, leukoaraiosis, osmotic stress, edema) are common in hemodialysis (HD) patients, but their etiologies are poorly understood. The acute effect of HD on blood biomarkers of brain injury has not yet been studied. We measured biomarkers for astroglial injury (GFAP, glial fibrillary acidic protein), axonal injury (NF-L, neurofilament-light), post-injury neurodegeneration (T-Tau, total Tau protein), and neuronal cell body injury (UCH-L1, ubiquitin C-terminal hydrolase-L1).

Methods

Three chronic HD patients (age 36±9 years; dialysis vintage 7±4 years) were enrolled in this one-week pilot study and dialyzed for 4 hours each on Monday, Wednesday, and Friday. Plasma samples were collected 6 times throughout each HD session. One study subject did not proceed after Monday HD and was withdrawn. A total of seven HD treatments were completed. GFAP, NF-L, T-Tau, and UCH-L1 were quantified by Neuro 4-Plex SIMOA assays (Quanterix, MA, USA). For biomarkers larger than 50kDa (GFAP, NF-L, and T-Tau), levels were corrected for hemoconcentration using total plasma protein levels.

Results

GFAP increased 2.1-fold by the end of HD (Fig 1a, p<0.001). NF-L (Fig 1b) and T-Tau (Fig 1c) results showed no conclusive change throughout HD. UCH-L1 decreased 0.8-fold by the end of HD (Fig 1d, p=0.03).

Conclusion

We report, for the first time, an increase of GFAP, a biomarker that is associated with astroglial injury, during routine HD. The results of our pilot study provide motivation to further explore the dynamics of brain injury biomarkers in HD patients to elucidate underlying mechanisms and aid research into neuro-protective interventions.