End Goals of Dialysis in Oxalic Acid Poisoning
The primary end goals of dialysis in acute oxalic acid poisoning are to normalize the anion gap to <18 mmol/L, achieve metabolic acidosis resolution with stable pH >7.35, and restore normal mental status—these three biochemical and clinical endpoints must all be met before discontinuing dialysis. 1, 2
Specific Biochemical Targets
The dialysis prescription must target concrete laboratory values rather than vague clinical improvement:
Anion gap normalization to <18 mmol/L is the primary biochemical endpoint, indicating adequate removal of oxalate and correction of the toxic metabolic derangement 1, 2
pH must stabilize above 7.35 with complete resolution of metabolic acidosis before considering dialysis cessation 1, 2, 3
Correction of acid-base abnormalities extends beyond simple pH normalization and requires achieving full metabolic stability 1
Critical Clinical Endpoints
Biochemical targets alone are insufficient—neurological recovery is mandatory:
Complete normalization of mental status is required, including resolution of altered consciousness, coma, or seizures that prompted dialysis initiation 1, 2, 3
Clinical improvement with stabilization of neurological function must be documented before stopping treatment 1
Why High-Flux Hemodialysis Achieves These Goals
The modality selection directly impacts the ability to reach these endpoints efficiently:
High-flux hemodialysis achieves oxalate clearance of 116 mL/min/1.73 m² BSA, which is vastly superior to peritoneal dialysis (7 mL/min/1.73 m²), allowing rapid removal of both parent compound and toxic metabolites 1, 2, 3
Technical specifications must include a high-flux membrane >1m² capillary surface area per 1m² body surface area and blood flow rate >250 mL/min to achieve these clearance rates 1, 2, 3
Intermittent hemodialysis with high-flux dialyzer is the preferred modality over continuous renal replacement therapy or peritoneal dialysis for acute poisoning 2, 3
Common Pitfalls in Endpoint Assessment
Do not stop dialysis based on clinical improvement alone—all three criteria (anion gap <18 mmol/L, pH >7.35, and mental status normalization) must be simultaneously met 1, 2, 3
Do not use peritoneal dialysis as it provides inadequate oxalate clearance and will not achieve endpoints in a timely manner 3
Do not delay dialysis waiting for traditional uremic indications—the anion gap >27 mmol/L and pH <7.1 thresholds are absolute indications regardless of other factors 2, 3
Context: Acute vs. Chronic Oxalate Toxicity
The endpoints differ dramatically based on poisoning type:
In acute oxalic acid poisoning, the goal is complete normalization of anion gap, pH, and mental status as described above 1, 2, 3
In chronic hyperoxaluria (a completely different clinical scenario), the goal is to target pre-dialysis plasma oxalate levels around 50-70 μmol/L to prevent systemic oxalosis, which differs substantially from acute poisoning endpoints 1, 3