What is the treatment for an adult with brake fluid poisoning and acute interstitial nephritis (inflammation of the kidney tissue) with impaired renal function?

Treatment of Brake Fluid Poisoning with Acute Interstitial Nephritis

Immediately discontinue the nephrotoxic exposure, initiate hemodialysis for the toxic glycol poisoning, and start IV methylprednisolone 1-2 mg/kg/day for the acute interstitial nephritis once the active toxic exposure is controlled. 1, 2

Immediate Stabilization and Toxin Management

The primary threat to life is the toxic glycol exposure from brake fluid, not the interstitial nephritis. Brake fluid contains toxic glycols and glycol ethers that cause severe metabolic acidosis, seizures, hypotension, and acute renal failure 3, 2.

Critical Initial Actions:

• Admit to ICU for ventilatory and inotropic support as brake fluid poisoning commonly causes coma, seizures, and cardiovascular collapse 3
• Initiate urgent hemodialysis for removal of toxic glycols—this is the definitive treatment for brake fluid poisoning presenting with metabolic acidosis and renal impairment 2
• Monitor for severe metabolic acidosis with increased anion gap and correct aggressively 3
• Rule out hypovolemia, urinary obstruction, and other concurrent nephrotoxic medications before confirming AIN as a contributing factor 4, 1

Grading the Acute Interstitial Nephritis Severity

Once the patient is stabilized from the acute toxic exposure, grade the AIN severity 4:

• Grade 3-4 AIN (creatinine ≥3× baseline or ≥4.0 mg/dL, or dialysis required) warrants the most aggressive immunosuppressive therapy 4, 1
• Grade 2 AIN (creatinine 2-3× baseline) requires close monitoring and consideration of steroids if no improvement after 5-7 days 4

Timing of Corticosteroid Therapy

This is the critical clinical decision point: The risk of immunosuppression must be weighed against the benefit of treating AIN 5.

Steroid Initiation Algorithm:

• Delay steroids until the toxic exposure is completely controlled and any secondary infections are treated 5
• Once the patient is stabilized from the acute poisoning (typically 24-48 hours), initiate IV methylprednisolone 1-2 mg/kg/day for Grade 3-4 AIN 4, 1
• If improvement occurs, transition to oral prednisone 1 mg/kg/day (maximum 80 mg/day) and taper over 4-12 weeks for severe cases 6, 1

The rationale: Infection-associated or toxin-associated AIN requires that steroids be delayed until active infection or ongoing toxic exposure is controlled, as immunosuppression during active toxicity significantly worsens outcomes 5.

Monitoring During Acute Phase

Check creatinine, electrolytes, and mental status daily during the acute treatment phase 1:

• Monitor for uremic encephalopathy which may manifest as confusion 1
• Correct electrolyte abnormalities and acid-base disturbances aggressively 1
• Assess fluid balance carefully, particularly if oliguria develops 6

Supportive Care During Steroid Therapy

If steroids are continued beyond 4 weeks 6, 1:

• Initiate Pneumocystis jiroveci pneumonia (PJP) prophylaxis 6, 1
• Provide calcium and vitamin D supplementation 6, 1
• Add gastric protection 6, 1
• Monitor afternoon glucose for hyperglycemia 6

Renal Replacement Therapy

Continue hemodialysis as needed based on:

• Persistent severe metabolic acidosis from glycol toxicity 2
• Uremic symptoms 1
• Severe electrolyte disturbances 1
• Fluid overload 6

Brake fluid poisoning cases have been successfully treated with hemodialysis even when presenting late 2.

Nephrotoxin Avoidance During Recovery

Permanently avoid re-exposure to brake fluid and strictly avoid all nephrotoxic medications during the recovery phase 6, 4:

• NSAIDs should be avoided entirely 6
• ACE inhibitors, decongestants, antivirals, antibiotics, and herbal products should be used with extreme caution 6
• Each additional nephrotoxin increases AKI odds by 53% 6

Common Pitfalls

The most critical error is initiating steroids before the toxic exposure is controlled, which can worsen outcomes in toxin-induced AIN 5. The second major pitfall is failing to initiate hemodialysis promptly for the glycol poisoning, focusing only on the AIN while the patient deteriorates from metabolic acidosis 2. Finally, delayed steroid initiation (beyond 5-7 days after toxin removal) is associated with poor renal recovery 7.

Prognosis

With appropriate treatment, renal function is usually reversible after the toxic exposure is treated and AIN is managed 5, 2. At 6 months, approximately 49% achieve complete recovery, 39% partial recovery, and 12% no recovery when steroids are used appropriately 7. Delayed diagnosis and delayed steroid initiation are the strongest predictors of poor recovery 7.