Acetate-Based Dialysate: The Middle Ages of Dialysis

Us renal fellows are likely to take for granted the fact that virtually all dialysis buffers used today are bicarbonate-based buffer systems. The bicarbonate-CO2 buffer system is the dominant buffer system in the human body, patients without renal function are often slightly acidotic, and therefore it makes sense that dialyzing a patient with a bicarbonate-based buffer system to restore bicarbonate levels to normal would be a naturally good idea.

However, bicarbonate-based dialysate has not always been the case! Up until the early 90s, the dominant form of dialysate buffer was an acetate-based dialysate. The reason that bicarbonate-based systems were not used at this time was because when mixed with any calcium, it would form an insoluble calcium bicarbonate compound; now there are systems which separate the acid (also containing the calcium) from the base (bicarbonate) and mix them just before use. According to multiple anecdotes from the more senior nephrology attendings & nurses at our hospital, most of the healthier patients would do relatively well with the acetate-based buffer systems--but those with liver failure, sepsis, or other severe illnesses would often feel extremely ill about an hour or so into acetate dialysis. This was in large part due to a defect in the ability to metabolically convert acetate to bicarbonate, and because bicarbonate was essentially being dialyzed off during dialysis, these patients could develop dangerous acidosis as a result. The effect is not unlike patients undergoing CVVH with a citrate-based replacement solution who have liver failure and are therefore unable to convert citrate to bicarbonate.

Another routine aspect of the dialysate which has changed is the calcium concentration of the dialysate. Previously, the tendency was to use a higher Ca concentration in the bath, between 3 or 3.5 mg/dL, in order to bring the post-dialysis serum calcium into the normal range. However now the current practice is to use a dialysate bath concentration of 2.25 or 2.5 g/dL, allowing the serum Ca concentration to remain slightly lower than the normal range with the idea that there will be less vascular calcification and (presumably) less cardiovascular mortality.