Question:medium
Which of these is NOT caused by amphotericin B?
Which of these is NOT caused by amphotericin B?
Show Hint
Amphotericin B damages renal tubules, not the glomerulus.
Updated On: Jul 8, 2026
- Azotemia
- Glomerulonephritis
- Hypokalemia
- Renal tubular acidosis
Show Solution
The Correct Option is B
Solution and Explanation
Step 1: Picture where the drug acts.
Amphotericin B has a strong attraction to cholesterol, and kidney tubule cell walls contain cholesterol too, so the drug injures these tubule cells as a side effect of killing fungi.
Step 2: Trace the tubule injury to its effects.
A damaged tubule leaks potassium into the urine, giving hypokalemia. It also loses the ability to pump out hydrogen ions, giving distal RTA. As tubular and vascular injury add up, the filtering capacity of the kidney drops, and urea and creatinine build up in the blood as azotemia.
Step 3: Separate this from glomerular disease.
Glomerulonephritis comes from inflammation and immune complex deposits at the glomerulus, a completely different part of the kidney and a different mechanism. Amphotericin B toxicity is a direct chemical injury to tubules, not an immune attack on glomeruli.
Step 4: Match to the options.
Azotemia, hypokalemia, and renal tubular acidosis are all documented amphotericin B effects. Glomerulonephritis is not, since the drug simply does not act at that site.
\[ \boxed{\text{Glomerulonephritis}} \]
Amphotericin B has a strong attraction to cholesterol, and kidney tubule cell walls contain cholesterol too, so the drug injures these tubule cells as a side effect of killing fungi.
Step 2: Trace the tubule injury to its effects.
A damaged tubule leaks potassium into the urine, giving hypokalemia. It also loses the ability to pump out hydrogen ions, giving distal RTA. As tubular and vascular injury add up, the filtering capacity of the kidney drops, and urea and creatinine build up in the blood as azotemia.
Step 3: Separate this from glomerular disease.
Glomerulonephritis comes from inflammation and immune complex deposits at the glomerulus, a completely different part of the kidney and a different mechanism. Amphotericin B toxicity is a direct chemical injury to tubules, not an immune attack on glomeruli.
Step 4: Match to the options.
Azotemia, hypokalemia, and renal tubular acidosis are all documented amphotericin B effects. Glomerulonephritis is not, since the drug simply does not act at that site.
\[ \boxed{\text{Glomerulonephritis}} \]
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