Abstract: TH-PO1132
Case of Amphotericin Induced Refractory Hypokalemia
Session Information
- Fluid, Electrolyte, Acid-Base Disorders
November 02, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Fluid, Electrolytes, and Acid-Base
- 704 Fluid, Electrolyte, Acid-Base Disorders
Authors
- Kozicky, Mark, Columbia University , New York, New York, United States
- Rao, Maya K., Columbia University , New York, New York, United States
- Stevens, Jacob, NYP Columbia - Nephrology Fellowship, New York, New York, United States
Background
Amphotericin (AmB) B is often used to treat severe fungal infections. It increases membrane permability of the renal tubular cell potentially leading to hypomagnesemia, hypokalemia and renal tubular acidosis. It also causes resistance to anti-diuretic hormone leading to polyuria that can potentiate hypokalemia by increasing distal urinary flow.
Methods
A 29 yr old male with sinonasal & intracranial aspergilloma infection was admitted to NICU in septic shock and respiratory failure requiring intubation. Despite anti-fungal treatment with micafungin, voriconazole, imaging showed growth of the fungal mass and treatment with AmB was initiated.
Within 2 days of starting amphotericin the patient developed new onset hypokalemia ranging from 2.3 to 3.4mmol/L with U waves seen on EKG. Hypokalemia remained refractory to supplementation over a week despite intravenous potassium repletion of ~ 200meq/ day plus an additional 40-100meq of oral KCl. Pt had some polyuria during this time with urine output(UOP) ranging from 1.5 - 5L daily in part driven by high input of ~ 5-6L/day, though UOP remained elevated over 2L/day even once IV hydration was reduced. While polyuria continued urine osmolarity ranged from 380 to 472 mOsm/kg demonstrating some persistent tubular concentrating function. Pt had no diarrhea noted and magnesium was supplemented to maintain adequate levels.
Diagnostic studies for hypokalemia including a cortisol level of 21.5ug/dL, renin & aldosterone levels of 0.38 ng/mL/h and 4.7ng/dL respectively were unremarkable upon evaluation of alternative causes of hypokalemia. 24 hour urinary potassium was elevated at 292 mmol/day while coincident serum potassium was 2.8mmol/L.
Due to refractory hypokalemia despite aggressive repletion and evidence of urinary potassium wasting, the patient started amiloride with slight improvement of potassium to ~3- 3.5mmol/L though not until AmB was discontinued after nearly 1 month of therapy did potassium levels normalize consistently to > 3.5mmol/L without further need of repletion and amiloride.
Conclusion
This case demonstrated amphotericin induced urinary potassium wasting via increased excretion along with polyuria refractory to high dose supplementation showing the potential harm & limitations in using AmB. It also demonstrates benefit of early initiation of potassium sparing diuretics to achieve potassium stabilization in patients requiring this medication.