Pseudoephedrine urolithiasis associated with acute renal failure

Charles L. Smith, Sheila K. Gemar and Matthew J. Lewis

Hennepin County Medical Center Division of Nephrology Minneapolis Minnesota USA Affiliated Community Medical Center Division of Urology Willmar Minnesota USA Email: smith156{at}umn.edu

Sir,

A 20-year-old male was taking ibuprofen for back pain and developed nausea, vomiting and peripheral oedema. His creatinine was 7.9 mg%. Renal ultrasound showed bilateral hydronephrosis. Ureteral stents were placed for probable papillary necrosis from ibuprofen and his creatinine fell to 1.1 mg%. Three months later his creatinine was 1.7 mg%. Renal ultrasound again showed hydronephrosis and an echogenic focus with shadowing. Plain X-rays of the abdomen were negative. Bladder calculi were found on cystoscopy and retrograde studies showed filling defects in the pelvis of the kidney. Recovered stone material was analysed and revealed 92% (Pseudo)ephedrine, 3% calcium phosphate and 5% protein. He had been taking pseudoephedrine for sinus headaches since age 9 years. Over the past 2 years he had increased the dose to 10, 60 mg tablets per day.

A 24-h urine sample was collected when his renal function was normal. His urine volume was 1125 ml/day. Urinary calcium excretion was 407 mg/day (NL <300 mg/day), oxalate 18 mg/day (NL <45 mg/day) and citrate 0.127 mmol/day (NL 1.861–4.303 mmol/day). He failed further follow-up.

This patient presented with acute renal failure from obstructive uropathy associated with radiolucent material composed of pseudoephedrine. Drug-induced urolithiasis is not uncommon [1] and there are previous reports of ephedrine containing renal stones usually accompanied by quaifenesin [25].

The 24-h urine collection revealed a low urine volume, hypercalciuria and hypocitraturia. Low urine volume is a recognized risk factor for all types of stone. Hypercalciuria is a risk factor for calcium stone disease and this patient had calcium phosphate as a part of his stones. However, the calcium phosphate was present in the intercrystalline voids suggesting it did not initiate stone formation but had precipitated on the pseudoephedrine. Hypocitraturia has been reported previously in patients with guaifenesin/ephedrine stones but the cause has not been investigated [4]. The patient failed to follow up before the hypocitraturia could be evaluated.

These stones can be added to the list of radiolucent stones and can be added to the growing list of drug-induced stones. It is characterized by frequent recurrence and may be associated with hypocitraturia. This type of stone disease will prove difficult to treat as it likely represents addiction to these stimulant drugs.

Conflict of interest statement. None declared.

References

  1. Hess B. Drug-induced urolithiasis. Curr Opin Urol 1988;8: 331–334[CrossRef]
  2. Blau JJ. Ephedrine nephrolithiasis associated with chronic ephedrine abuse. J Urol 1998;160 [3 Pt 1]: 825
  3. Powell T, Hsu FF, Turk J, Hruska K. Ma-Huang strikes again: ephedrine nephrolithiasis. Am J Kidney Dis 1998;32: 153–159[ISI][Medline]
  4. Assimos DG, Langenstroer P, Leinbach RF, Mandel NS, Stern JM, Holmes RP. Guaifenesin- and ephedrine-induced stones. J Endourol 1999;13: 665–667[ISI][Medline]
  5. Pickens CL, Milliron AR, Fussner A et al. Abuse of guaifenesin-containing medications generates an excess of a carboxylate salt of beta-(2-methoxyphenoxy)-lactic acid, a guaifenesin metabolite, and results in urolithiasis. Urology 1999;54: 23–27[CrossRef][ISI][Medline]




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