Step 1: Understanding the Concept:
Amphotericin B is a polyene antifungal that binds ergosterol in fungal membranes, but it also binds cholesterol in human cell membranes, and this cross-reactivity is what damages the kidney.
Step 2: Key Formula or Approach:
When amphotericin B binds cholesterol in the distal renal tubular cell membrane, it forms pores that let small ions leak out of the cell into the urine, so the electrolytes affected are the ones normally reabsorbed at the distal tubule.
Step 3: Detailed Explanation:
Potassium and magnesium are the two ions most affected by this pore formation, and both are lost into the urine instead of being reabsorbed.
Sodium and calcium handling are not driven by the same distal tubular pores, so they are not the drug's main electrolyte effect.
Of potassium and magnesium, potassium loss is the one that shows up clinically first and most often, producing low serum potassium along with muscle weakness and a risk of arrhythmia.
This renal potassium wasting is severe enough that patients on amphotericin B are usually monitored and often supplemented with potassium during treatment.
Step 4: Final Answer:
Amphotericin B is associated with hypokalemia.