ABSTRACT
When renal replacement therapy is initiated, regulation of body HCO3
stores shifts from a failing biological system (see Chapter 14) to a new process regulated solely by the physical principles of diffusion and convection (1). This switch has major implications for acid-base homeostasis, changing the way one thinks both about both normal and disordered acid balance. In contrast to individuals with functioning kidneys where HCO3
stores are continuously replenished by changes in acid excretion to match endogenous production, individuals with end-stage renal disease require exogenous alkali to maintain body stores. Alkali repletion is most often accomplished by adding either HCO3
or a HCO3 precursor to the dialysis bath solution.
With some forms of therapy, HCO3 is given intravenously. Regardless of
the approach, alkali addition causes a unique new equilibrium to develop in which a biological homeostatic process involving sensors and effectors is replaced by a process determined by factors influencing the movement of HCO3
