Dialysis Initiation in Oxalic Acid Poisoning
Initiate hemodialysis immediately in acute oxalic acid poisoning when pH <7.1, anion gap >27 mmol/L, acute kidney injury (KDIGO stage 2 or 3), or altered mental status including seizures or coma. 1
Clinical Indications for Immediate Dialysis
The decision to initiate dialysis in oxalic acid poisoning differs fundamentally based on whether the exposure is acute poisoning versus chronic hyperoxaluria (such as primary hyperoxaluria).
Acute Oxalic Acid Poisoning
Immediate dialysis is indicated when any of the following are present:
- Severe metabolic acidosis: pH <7.1 or anion gap >27 mmol/L 1
- Acute kidney injury: KDIGO stage 2 or 3 1
- Neurological manifestations: Coma, altered consciousness, or seizures 1
- Osmolal gap: >50 mOsm/L when oxalic acid exposure is confirmed 1
Lower threshold for dialysis initiation:
- Pre-existing chronic kidney disease with eGFR <45 mL/min/1.73m² 1
The rationale is straightforward: direct oxalic acid ingestion causes rapid metabolic acidosis and acute tubular damage from calcium oxalate crystal deposition in renal tubules 2, 3. These patients develop life-threatening complications within hours and require urgent intervention to prevent mortality.
Chronic Hyperoxaluria (Primary Hyperoxaluria)
Consider intensified dialysis before traditional uremic indications when:
- Plasma oxalate exceeds 30 μmol/L despite oxalate-lowering therapy (pyridoxine or RNAi therapy), even if GFR would not typically warrant dialysis 4
- Signs of systemic oxalosis are present with stage 4-5 CKD 5
- High plasma oxalate levels persist, indicating tissue storage risk 5
This represents a fundamentally different clinical scenario where dialysis serves as a bridge to liver transplantation rather than acute life-saving intervention. Regular dialysis regimens remove only 1.0-1.4 mmol oxalate daily, insufficient to counteract the 4-7 mmol daily production in PH1 5.
Dialysis Modality and Prescription
Use intermittent hemodialysis with high-flux dialyzer as the preferred modality over continuous renal replacement therapy or peritoneal dialysis. 1
Technical Specifications for Acute Poisoning:
- High-flux membrane: >1m² capillary surface area per 1m² body surface area 1
- Blood flow rate: >250 mL/min (or >150-200 mL/min/m² BSA in children) 1
- Rationale: High-flux hemodialysis achieves oxalate clearance of 116 mL/min/1.73 m² BSA versus only 7 mL/min/1.73 m² with peritoneal dialysis 1
Intensive Dialysis for Chronic Hyperoxaluria:
- Frequency: Daily hemodialysis sessions if tolerated, potentially combined with nocturnal peritoneal dialysis 5
- Target: Pre-dialysis plasma oxalate levels around 50-70 μmol/L 5, 4
- High-flux dialyzer with maximal blood flow 5, 4
Six 4.5-hour hemodialysis sessions per week with high-flux filter can remove 24 mmol/1.73 m² per week, approaching the estimated weekly oxalate production of 28-37.7 mmol 5.
Cessation Criteria for Acute Poisoning
Stop dialysis when all of the following are achieved:
- Anion gap normalizes to <18 mmol/L 1
- Metabolic acidosis resolves with stable pH >7.35 1
- Clinical improvement with normalization of mental status 1
Common Pitfalls to Avoid
- Do not delay dialysis waiting for traditional uremic indications in acute poisoning—the anion gap and pH thresholds are absolute indications 1
- Do not use peritoneal dialysis as first-line modality in acute poisoning due to inadequate oxalate clearance 1
- Do not assume standard thrice-weekly dialysis is sufficient in chronic hyperoxaluria—systemic oxalate accumulation will continue 5
- Do not overlook pre-existing kidney disease as this significantly lowers the threshold for dialysis initiation in acute poisoning 1
The key distinction is recognizing that acute oxalic acid poisoning requires emergency dialysis based on metabolic parameters and neurological status, while chronic hyperoxaluria requires preemptive intensive dialysis based on plasma oxalate levels to prevent systemic oxalosis.