In patients on hemodialysis, the reduced alkali urinary loss makes metabolic acidosis less severe. Unexpected is the large occurrence of respiratory alkalosis and acidosis.
During the therapy, the convective/diffusive inward fluxes of CO2 and bicarbonate and the loss of organic anions affect acid-base homeostasis.
In bicarbonate-dialysis, the neutralization of acids by bicarbonate and gain of gaseous CO from the dialysate cause an increase of CO2 content in the body water, which requires an increase in lung ventilation (>10%) to prevent hypercapnia. In on-line hemodiafiltration, the infusate drags additional CO2 into bloodstream, while in acetate – free biofiltration the dialysate is CO2 – free and this prevents any addition of CO2.
Bicarbonate and acetate diffuse into extracellular fluid according to their bath-to-blood concentration gradients. The initially large bicarbonate flux decreases rapidly because of the rapid increase in blood concentration. The smallest acetate flux is instead constant with time providing a constant source of alkali.
Rapid alkalinization elicits H+ mobilization that consumes most of the bicarbonate added. Some H+ are originated by back-titration of body buffers, but others are originated by new organic acid production, a maladaptive event that wastes metabolic energy. In addition, organic anions diffuse into dialysate causing a substantial increase in net acid production.
A novel dialysis protocol prescribes a low initial bath bicarbonate concentration and a stepwise increase during the therapy. Such a staircase protocol ensures a smoother increase of blood bicarbonate concentration avoiding the initial rapid growth and reducing the rate of organic acid production, thus making the treatment more effective.
Keywords: Acid-base, Bicarbonate, Carbon Dioxide, Dialysate, Hemodialysis