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

Abstract

This study contrasts the abilities and mechanisms of two physicochemical, mathematical models to predict experimental bicarbonate kinetics, hence, buffer transport, during a hemodialysis (HD) treatment in chronic renal failure patients. The existing Sargent model assumes that the body fluids can be described as a single, homogeneous extracellular fluid (EC) compartment whose volume decreases because of a constant ultrafiltration rate during HD. Bicarbonate and acetate transport between HD fluid and the EC compartment are by convection and diffusion with acetate metabolized in that compartment. The new model formulated in this study assumes the same conditions as Sargent et al., but constrains ion concentrations in the EC to be electrically neutral at all times. This constraint requires inclusion in the EC of other transportable small ions, Na+, K+, Cl- and unidentified, anionic organic acids in addition to an electrical charge on impermeable albumin. The findings are that the new electroneutrality model predicts plasma bicarbonate-concentration kinetics as closely as the Sargent model, but bicarbonate transport is an unlikely mechanism. Rather, the findings are better explained by rapid interconversion of CO2 and bicarbonate in this simplified EC compartment model. The results of this study bring into question the ability of the Sargent et al. hypothesized H+-mobilization model to explain buffer-transport kinetics during HD.