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Abstract: FR-PO446

Acid-Base Dynamics in Allo-Hemodialysis Treatments: Quantitative Insights from a Novel Physiology-Based Mathematical Model

Session Information

Category: Dialysis

  • 701 Dialysis: Hemodialysis and Frequent Dialysis

Authors

  • Cherif, Alhaji, Renal Research Institute , New York, New York, United States
  • Maheshwari, Vaibhav, Renal Research Institute , New York, New York, United States
  • Thijssen, Stephan, Renal Research Institute , New York, New York, United States
  • Kotanko, Peter, Renal Research Institute , New York, New York, United States
Background

In some areas of the world access to conventional hemodialysis (HD) is elusive, resulting in millions of premature deaths every year. Allo-hemodialysis (alloHD) is a substantially simplified and less costly dialysis modality, in which the blood of a healthy subject (“buddy”) flows counter-current to the patient’s blood through the dialyzer. Solutes, including bicarbonate, are transferred across the membrane. In this study, we proposed a physiology-based mathematical model to explore the impact of alloHD on the patient’s and buddy’s acid-base status.

Methods

A dynamic model of physiological regulation of HCO3/CO2 buffering system with Henderson-Hasselbalch mass-action kinetics is used to describe a coupled transfer between patient and buddy via alloHD. The model incorporates production of CO2 and H+, loss due to non-bicarbonate buffering, and ventilation. In addition, we assume a normal renal function and regulation of HCO3/CO2 in the buddy, but not in the patient. The patient model is parameterized to yield various degrees of metabolic acidosis, while the buddy model is parameterized to physiological values.

Results

Figure 1 shows an example of acid-base dynamics. AlloHD is able to correct patients’ acid-base status. Interestingly, there are only minimal changes to the buddy’s acid-base status. The buddy’s kidney function affects the extent to which the patient’s acid-base status is corrected. Furthermore, since buddy’s renal function is fully intact, we observe a secondary compensation where HCO3, pCO2 and pH initially decrease before regulatory compensations restore the buddy’s acid-base status.

Conclusion

Our findings indicate that an alloHD session can restore the patient’s acid-base status. Our modeling suggests that there is minimal disturbance in buddy’s acid-base status while providing substantial corrective regulation of patient’s acid-base homeostasis. Although our modeling results are promising, there is a need for further empirical investigation to verify the predictive power of the model.

Figure 1: Temporal dynamics of acid-base status in patient and buddy during alloHD