Choice of replacement fluid/dialysate anion in continuous renal replacement therapy

Abstract

Normalization of acid-base balance in patients with acute renal failure (ARF) is a primary goal of continuous extracorporeal renal replacement therapy (CRRT). During CRRT, alkali administration, either in the replacement fluid or by diffusive uptake from the dialysate, must replace not only the bicarbonate lost in the buffering of endogenous acid production, but also the bicarbonate lost across the hemodiafilter. In most patients with ARF, a buffer concentration of approximately 30 to 35 mmol/L and an ultrafiltration rate (or dialysate flow rate) approaching or exceeding 1 L/hr can be expected to normalize the acid-base status within 1 to 2 days. In individuals with ARF and lactic acidemia, the buffer load may need to approach ≥50 mmol/L to correct the associated metabolic acidemia. Acetate, bicarbonate, citrate, and lactate are the possible choices for bicarbonate or bicarbonate-equivalent administration during CRRT. Acetate- and lactate-based physiologic solutions have the advantage of being commercially available. Under normal conditions, acetate and lactate are metabolized rapidly to bicarbonate. Under conditions where the conversion pathways may be impaired, such as in severe hypoxic or shock states, excessive accumulation of these anions is possible. In the latter situation, the rate of anion conversion to bicarbonate may be slower than the rate of bicarbonate loss across the hemodiafilter, and a worsening of metabolic acidemia may occur. In addition, the administration of large amounts of lactate may result in increased urea generation. Bicarbonate has the major advantage of being the most physiologic anion. Unfortunately, the production of a commercially available bicarbonate-based physiologic solution is difficult because of the loss of bicarbonate from the solution or the formation of calcium and magnesium salts. The use of citrate as an anticoagulant obviates the need for additional alkali because citrate is metabolized to bicarbonate. Excessive citrate accumulation is rare, even in the setting of severe hepatic failure.