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Abstract: PO0943

Effect of Hemodialysis on Amyloid-β in Cerebrospinal Fluid and Plasma

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
  • Chao, Joshua Emmanuel, Renal Research Institute, New York, New York, United States
  • Patel, Amrish U., Renal Research Institute, New York, New York, United States
  • Debure, Ludovic, NYU Langone Health, 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
  • Zhang, Hanjie, 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

Hemodialysis (HD) can reduce amyloid-beta (Aβ) species in whole-body circulation by 30 to 50%. Due to the dynamic exchange of Aβ between the brain and the blood, we hypothesized that HD might lower Aβ levels in the cerebrospinal fluid (CSF).

Methods

In a dialysis network with over 160,000 patients, we identified three maintenance HD patients (age 36±9 years) with ventriculo-peritoneal (VP) shunts who were subsequently recruited for this IRB-approved research study. Study subjects were dialyzed on Monday, Wednesday, and Friday. Plasma samples were collected at 6 timepoints during the 3 HD sessions. One subject was withdrawn over safety concern related to the VP shunt tap procedure. Two subjects further underwent VP shunt taps for CSF sample collection before and after the Wednesday and Friday HD sessions, and once on interdialytic days (Tuesday, Thursday). Aβ1-42 and Aβ1-40 were quantified by Neuro 3-Plex SIMOA assays (Quanterix, MA, USA).

Results

HD effectively reduced plasma Aβ1-40 by 41% and Aβ1-42 by 34% (Fig 1a and 1b, p < 0.01). In CSF, levels of Aβ increased after Wednesday HD sessions in subject 1 (Aβ1-40: 4.2-fold, Aβ1-42: 5.5-fold) and subject 2 (Aβ1-40 and Aβ1-42: 1.06-fold), while Aβ decreased after Friday HD sessions in both subject 1 (Aβ1-40: 0.1-fold, Aβ1-42: 0.1-fold) and 2 (Aβ1-40: 0.7-fold, Aβ1-42: 0.7-fold) shown in Figure 1c–f.

Conclusion

This is the first report of Aβ dynamics in the CSF and plasma of HD patients. While plasma levels were in similar ranges, we found high inter-individual variations of CSF levels. Different plasma-to-CSF ratios after HD may reflect individual brain Aβ pools that are accessed by HD. We corroborate previous reports demonstrating the removal of Aβ from the blood compartment by HD.