Mechanisms of Acid-Base Kinetics During Hemodialysis: a Mathematical-Model Study.

Area of Science:

• Physicochemical modeling
• Renal physiology
• Biomathematics

Background:

• Chronic renal failure impairs buffer regulation.
• Hemodialysis (HD) aims to restore acid-base balance.
• Existing models for HD buffer transport have limitations.

Purpose of the Study:

• To compare two mathematical models for predicting bicarbonate kinetics during HD.
• To investigate the mechanisms of buffer transport in chronic renal failure patients undergoing HD.
• To evaluate the validity of the Sargent model's H+-mobilization hypothesis.

Main Methods:

• Developed a new physicochemical, mathematical model incorporating electroneutrality constraints.
• Assumed a single, homogeneous extracellular fluid (EC) compartment with ultrafiltration.
• Modeled bicarbonate and acetate transport via convection and diffusion.

Main Results:

• The new electroneutrality model accurately predicted plasma bicarbonate kinetics, similar to the Sargent model.
• Bicarbonate transport was deemed an unlikely mechanism for observed kinetics.
• Rapid interconversion of CO2 and bicarbonate within the EC compartment better explains the findings.

Conclusions:

• The electroneutrality model provides a comparable prediction of bicarbonate kinetics to the Sargent model.
• The study questions the Sargent model's H+-mobilization hypothesis for buffer transport during HD.
• CO2-bicarbonate interconversion is a more plausible explanation for buffer kinetics in this context.