A patient with a systemic fungal infection is treated with amphotericin B deoxycholate. After 5 days she develops rising serum creatinine, hypokalaemia, and hypomagnesaemia. Which mechanism best explains these electrolyte abnormalities?
- A Amphotericin B binds sterols in renal tubular membranes, forming pores that increase ion permeability and potassium/magnesium wasting ✓
- B Amphotericin B inhibits the Na-K-ATPase pump in renal tubular cells
- C Amphotericin B inhibits carbonic anhydrase in the proximal tubule
- D Amphotericin B activates mineralocorticoid receptors, causing potassium wasting
Correct answer: A. Amphotericin B binds sterols in renal tubular membranes, forming pores that increase ion permeability and potassium/magnesium wasting
Explanation
Amphotericin B binds ergosterol in fungal membranes to form pores. Mammalian cell membranes contain the related sterol cholesterol, and in renal tubular cells amphotericin forms similar pores causing increased permeability to cations, leading to potassium and magnesium wasting in the distal nephron. The resulting nephrotoxicity and electrolyte depletion require close monitoring and supplementation. Liposomal formulations reduce renal tubular exposure and are less nephrotoxic.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.