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Clinical Pharmacy Specialist, Division of Pharmacy, Unit 90, The University of Texas MD Anderson Cancer Center, Houston, TX
Critical Care Physician, Division of Critical Care/Anesthesiology, Unit 42, The University of Texas MD Anderson Cancer Center
Clinical Pharmacy Specialist, Department of Pharmacy, Barnes-Jewish Hospital, St. Louis, MO
Reprints: Todd W Canada PharmD BCNSP, Division of Pharmacy, Unit 90, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030-4009, FAX 713/794-4399, E-mail tcanada{at}mdanderson.org
OBJECTIVE: To report the development of nephrogenic diabetes insipidus (NDI) associated with the use of high-dose liposomal amphotericin B.
CASE SUMMARY: A 38-year-old white man with relapsed acute myelogenous leukemia underwent a matched unrelated donor allogeneic bone marrow transplant with adequate engraftment and mild graft-versus–host disease responding to corticosteroids. Approximately 11 months after transplant, the patient was admitted to the hospital with suspected fungal pneumonia and started on liposomal amphotericin B (baseline serum creatinine 1.4–1.5 mg/dL). The dose was increased due to his immunosuppression and poor response, as the fungal etiology was identified as Torulopsis glabrata. The patient required mechanical ventilation due to biopsy-proven bronchiolitis olbiterans organizing pneumonia. Additionally, he developed diffuse alveolar hemorrhage and received intravenous desmopressin, with a reduction in bloody secretions. He also developed hypernatremia (serum sodium 155 mEq/L) on day 3 of the desmopressin and had an inappropriately increased urine output consistent with NDI. The most likely etiology for the NDI was liposomal amphotericin B and its associated hypokalemia.
DISCUSSION: The observation of worsening hypernatremia (serum sodium increased from 135 to 164 mEq/L) with polyuria was associated with an increasing cumulative dosage of liposomal amphotericin B for fungal pneumonia despite the concurrent use of intravenous desmopressin. Aggressive water replacement was an effective treatment option in this patient. The Naranjo probability scale classified this as a possible adverse reaction because of the temporal sequence of NDI after high-dose liposomal amphotericin B and previously reported cases of NDI associated with amphotericin B desoxycholate.
CONCLUSIONS: Amphotericin B desoxycholate has been implicated as an etiology for NDI, and the use of the newer liposomal amphotericin B reportedly avoids this rare complication. We observed the development of NDI despite the use of liposomal amphotericin B in a critically ill patient with bone marrow transplant.
Key Words: liposomal amphotericin B, nephrogenic diabetes insipidus
www.theannals.com, DOI
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