ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2019 and some content may be unavailable. To unlock all content for 2019, please visit the archives.

Abstract: SA-PO224

Hemodialysis Augments Red Blood Cell Death and Intracellular Hypoxia

Session Information

Category: Anemia and Iron Metabolism

  • 201 Anemia and Iron Metabolism: Basic

Authors

  • Dias, Gabriela Ferreira, Pontifícia Universidade Católica do Paraná/PUCPR, Curitiba, PR, Brazil
  • Andrade, Gabriela Bohnen, Pontifícia Universidade Católica do Paraná, Curitiba, Brazil
  • Tozoni, Sara Soares, Pontifícia Universidade Católica do Paraná, Curitiba, PR, Brazil
  • Grobe, Nadja, Renal Research Institute, New York, New York, United States
  • Pecoits-Filho, Roberto, Arbor Research Collaborative for Health, Ann Arbor, Michigan, United States
  • Kotanko, Peter, Renal Research Institute, New York, New York, United States
  • Moreno-Amaral, Andrea Novais, Pontifícia Universidade Católica do Paraná/PUCPR, Curitiba, PR, Brazil
Background

Previous studies have shown that uremia increases red blood cell (RBC) death (eryptosis) in hemodialysis (HD) patients, possibly aggravating their anemia. The present study tests the hypothesis that hemodialysis (HD) triggers eryptosis, as indicated by phosphatidylserine (PS) exposure, and calcium influx into RBC. In addition, we explored levels of RBC intracellular hypoxia.

Methods

RBC were obtained from healthy subjects (CON-RBC; n=8) and ESRD patients (HD-RBC; n=10) pre- and post-HD. Using flow cytometry, PS exposure (Annexin-V), calcium influx (Fluo 3-AM probe), and intracellular level of hypoxia (Hypoxia Green probe) were determined. Results are expressed in mean fluorescence units (MFI). We compared these parameters between healthy controls and pre- and post-HD, respectively.

Results

The age of the healthy subjects was 34.8±17.3 years, 20% were male. The patients were 73% males, the age was 58.1±18.1 years. Compared to CON-RBC, PS exposure, calcium influx, and levels of intracellular hypoxia were increased in HD-RBC pre- and post-HD, respectively. In addition, HD treatment was associated with significantly increased PS exposure and intracellular hypoxia (Table 1).

Conclusion

Taken together, our results suggest that HD increases RBC hypoxia, eryptosis, and RBC calcium influx. Lower oxygen levels in HD-RBC could be due to either an impaired uptake or enhanced release of oxygen. Oxygen-sensitive intracellular responses may regulate RBC lifespan.

Eryptosis and oxygen levels in RBC from healthy controls (CON-RBC) and hemodialysis patients (HD-RBC) pre- and post-HD.
Parameters
[in MFI units]
CON-RBC
(n=8)
HD-RBC
Pre-HD (n=10)
HD-RBC
Post-HD(n=10)
Ca2+ influx31.9±14.660.9±17.4***74±15.8***
PS exposure2.6±1.612.5±6**27.2±7.2*** (#)
Hypoxia level9.7±2.314.63±3.3*22.15±4.9***(#)

Data are shown as mean±SD of the Mean Fluorescence Intensity (MFI). *p<0.05, **p<0.01, ***p<0.001 correspond to the difference between HD-RBC and CON-RBC. (#) p<0.01 corresponds to the difference between pre-HD-RBC and post-HD-RBC.