Dialysis-Related Acidemia and Acidosis by Dialysate: The Forgotten Issue of CO2 Overload from Dialysate.

blood returning to the patient [2–4, 8] . This hypercapnia lowers pH despite high bicarbonate concentration but without hypoxia, unless lung disease coexists. The added CO 2 normally is quickly removed by respiration and systemic pCO 2 remains essentially unaffected. Having said that, ‘dialysis-related acidemia’ is the typical acid-base pattern of blood exiting the filter (venous line) in bicarbonate dialysis (fig. 1a). If dialysis-related acidemia is found in the arterial line, then vascular access should be inspected for correct needle placement or fistula malfunction because recirculation occurs when blood exiting the filter is not flowing into systemic blood but is reentering the extracorporeal circuit [9] . A more serious problem can occur if dialysisrelated acidemia of venous line is coupled with underlying pulmonary or cardiac disease. If the patient is unable to breath away the CO 2 added from the dialysate (fig. 1b), then hypercapnic acidosis will occur or be exacerbated [2, 4] . In such a case, the label ‘acidosis by dialysate’ should be used because the mixed acidosis found in the arteDear Editor, During hemodialysis, the arterial line of the extracorporeal circuit allows for easy access to arterial blood sampling [1] , but may return unexpected findings. We would like to briefly comment on the unique acid-base pattern featured by high partial pressure of carbon dioxide (pCO 2 ) not associated with hypoxia. Hypercapnia causes a decrease in pH. At a glance, hypercapnic acidemia calls up respiratory acidosis, but hypercapnia from lung failure is closely associated with hypoxia. There is another circumstance of hypercapnia featured by normal oxygenation and lung function. This non-hypoxic hypercapnic acidemia may be called ‘dialysisrelated acidemia’ [2–4] . During bicarbonate-dialysis there is a gain of CO 2 [5] . After mixing of the acid concentrate with the bicarbonate-containing solution, the pCO 2 in the dialysate ranges between 80 and 100 mm Hg [3, 6, 7], whereas arterial pCO 2 commonly is below 40 mm Hg (as a result of the ventilatory response to the metabolic acidosis in kidney failure). This leads to high CO 2 dialysance and thus to a sizable increase in pCO 2 in Received: October 23, 2015 Accepted: January 21, 2016 Published online: February 6, 2016