Can Lactate Be Cleared by Dialysis?
Yes, lactate can be cleared by dialysis, but the contribution of dialysis to total lactate clearance is minimal (typically <3% of total body lactate clearance) and should not be relied upon as a primary mechanism for treating hyperlactatemia. 1
Quantitative Evidence on Lactate Clearance by Dialysis
Continuous Renal Replacement Therapy (CRRT)
- Filter lactate clearance during continuous venovenous hemofiltration with dialysis (CVVHD) is approximately 24 mL/min (range 7-36 mL/min), which represents less than 3% of total body lactate clearance of approximately 1379 mL/min in critically ill patients. 1
- Peritoneal dialysis provides even lower lactate clearance at approximately 9 mL/min, though it can remove between 88-352 mEq of total lactate during a dialysis session. 2
Clinical Implications
- Because dialytic lactate clearance is negligible compared to endogenous metabolism, lactate levels remain a reliable marker of tissue oxygenation and shock even in patients receiving renal replacement therapy. 1
- The body's endogenous lactate metabolism capacity far exceeds what any dialysis modality can achieve, meaning dialysis cannot mask lactate overproduction from tissue hypoperfusion. 1
Critical Guideline Recommendations on Lactate-Buffered vs. Bicarbonate-Buffered Dialysate
Strong Recommendations Against Lactate-Based Solutions in Specific Populations
The KDIGO guidelines strongly recommend (1B) using bicarbonate rather than lactate as a buffer in dialysate and replacement fluid for patients with AKI and circulatory shock. 3, 4
For patients with AKI and liver failure and/or lactic acidemia, bicarbonate is suggested (2B) over lactate-buffered solutions. 3, 5, 4
Rationale for Avoiding Lactate-Buffered Solutions
- In patients with liver failure or lactic acidosis, lactate-containing dialysis solutions may worsen acidosis rather than improve it, as the liver cannot efficiently convert the exogenous lactate load to bicarbonate. 5
- Lactate-buffered CRRT can cause hyperlactatemia in all patients, with less than 40% of acute renal failure patients showing the expected improvement in acid-base status (increased bicarbonate, reduced hydrogen ions). 6
- A positive correlation exists between increased arterial lactate and hydrogen ion concentrations (r=0.52, p<0.01) when using lactate-buffered solutions, potentially worsening acidosis. 6
Comparative Effectiveness: Lactate-Free vs. Lactate-Buffered Dialysate
Acid-Base Control
- Lactate-free (bicarbonate-based) dialysate provides more rapid control of acidosis than lactate-buffered dialysate in patients with multi-organ failure. 7
- Bicarbonate-based solutions require less total buffer administration compared to lactate-buffered solutions. 7
Hemodynamic Stability
- Mean arterial pressure rises during lactate-free dialysis with decreased inotrope requirements, while it falls during lactate-buffered dialysis with increased inotrope needs. 7
- This hemodynamic advantage occurs regardless of whether patients have liver dysfunction. 7
Lactate Accumulation
- While lactate accumulation is generally slight with both approaches over 24 hours in patients with multi-organ failure, it is higher during lactate-buffered CVVHD. 7
- Lactate accumulation in critically ill patients near their threshold for lactate utilization may further depress cardiac function and peripheral lactate metabolism. 6
Clinical Pitfalls and Caveats
Common Misconception
- Do not rely on dialysis to "clear" elevated lactate levels in shock or sepsis—the primary treatment must address the underlying cause of lactate production (tissue hypoperfusion, sepsis, etc.). 3, 1
Monitoring Requirements
- When using lactate-buffered solutions in critically ill patients, arterial pH must be monitored so that bicarbonate solutions can be substituted if acid-base status progressively worsens. 6
- Lactate levels remain valid for monitoring tissue perfusion and shock severity even during dialysis. 1