A 22-year old white male is seen in the emergency room at midnight for evaluation of acute renal failure. He explains that he finished running the Boston marathon 8 hrs previously. He complains of severe leg cramps. He tells you that he has had no urine output. No significant past medical history. No medications. Denies recent alcohol consumption. PE: BP 120/80 mmHg, HR110 bpm, afebrile. JVP is 2-3 cm. Clear lungs, normal cardiovascular and abdominal examination. No edema. Skin turgor reduced. Urinalysis: SG of 1020, pH 5.0, 4+ blood, rest negative. What is the next step in management:
–A.) He should be assured that this presentation is common in marathon runners and he will improve with bed-rest
–B.) He should be treated with high dose ibuprofen (800 mg TID until his leg cramps resolve).
–C.) He should be rapidly volume repleted with normal saline
–D.) He should be immediately administered 10 g mannitol IV
–E.) Furosemide 120 mg IV should be given immediately
______________________The correct answer for the AKI Quiz 10/9/11 is C. The biopsy shows numerous crystalline inclusions consistent with calcium oxalate.
32 yo man presented with kidney failure. His tox screen was positive for cocaine. He was normotensive and physical exam was unremarkable. BUN was 52 mg/dL and Cr 8.1 mg/dL. Sodium was 139 mEq/L, potassium 4.9 mEq/L, chloride 103 mEq/L and bicarbonate 17 mEq/L. Calcium was 8.0, Urinalysis had 1+ protein, 3-5 WBC/hpf and 1-3 RBC/hpf. Envelope shaped and needle-like crystals were noted on sediment. Renal ultrasound was negative for obstruction.
The renal biopsy proves that the diagnosis is:
A. Kappa light chain cast nephropathy
B. Acute phosphate nephropathy
C. Ethylene glycol toxicity
D. Primary hyperoxaluria, Type I
E. Rhabdomyolysis
Explanation
Ethylene glycol toxicity can present clinically in the following ways:
Ethylene glycol toxicity can present clinically in the following ways:
• AKI
• High anion gap acidosis
• Osmolar gap - usually
• Oxalate crystals on sediment (letter shaped or needle-like birefringent)
• Hypocalcemia
Ethylene glycol is metabolized to glycoaldehyde and glyoxalate – these are tubular toxins that can cause AKI; ethylene glycol is also metabolized to calcium oxalate monohydrate crystal deposition that can result in intratubular obstruction.
Treatment relies on the use of fomepizole (an alcohol dehydrogenase inhibitor), hemodialysis, and the potential use of intravenous alcohol (if fomepizole is unavailable).
References
Stokes MB. Acute oxalate nephropathy due to ethylene glycol ingestion. Kidney Int. 2006 Jan;69(2):203. PubMed PMID: 16408105.
Keiran S, Bhimani B, Dixit A. Ethylene glycol toxicity. Am J Kidney Dis. 2005 Sep;46(3):e31-3. PubMed PMID: 16134263.
