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Difficulty: MediumNephrology

Match each commonly prescribed medication with its primary mechanism of inducing acute kidney injury (AKI).

  • GentamicinDirect toxic injury to proximal tubular epithelial cells
  • IbuprofenInhibition of vasodilatory prostaglandins leading to afferent arteriolar vasoconstriction
  • NafcillinIdiosyncratic delayed hypersensitivity reaction in the renal interstitium
  • Intravenous AcyclovirPrecipitation of insoluble metabolites causing intratubular obstruction

Answer

Gentamicin causes direct tubular toxicity (ATN). Ibuprofen causes hemodynamically mediated AKI via afferent vasoconstriction. Nafcillin induces an allergic acute interstitial nephritis (AIN). Intravenous acyclovir causes intratubular obstruction via crystal precipitation.
Each medication listed corresponds to a distinct pathophysiological mechanism of acute kidney injury. Aminoglycosides (gentamicin) directly damage the proximal tubule resulting in ATN. NSAIDs (ibuprofen) block the synthesis of vasodilatory prostaglandins, leading to afferent arteriolar vasoconstriction and decreased GFR (prerenal/hemodynamic AKI). Beta-lactams (nafcillin) act as haptens to trigger an allergic, cell-mediated immune response in the renal interstitium (AIN). Acyclovir, particularly when administered intravenously without adequate hydration, crystallizes within the tubular lumen, causing crystal-induced intrarenal obstruction.

Step-by-Step Solution

1
Identify the mechanism of aminoglycoside-induced nephrotoxicity.
Gentamicin causes direct toxic injury to proximal tubular epithelial cells (Acute Tubular Necrosis).
Aminoglycosides accumulate in the proximal tubule cells, leading to cellular necrosis and sloughing into the tubular lumen (muddy brown casts).
2
Identify the mechanism of NSAID-induced nephrotoxicity.
Ibuprofen causes inhibition of vasodilatory prostaglandins leading to afferent arteriolar vasoconstriction.
Prostaglandins normally dilate the afferent arteriole to maintain glomerular filtration rate (GFR). NSAIDs block this, reducing renal blood flow.
3
Identify the mechanism of penicillin-induced nephrotoxicity.
Nafcillin causes an idiosyncratic delayed hypersensitivity reaction in the renal interstitium (Acute Interstitial Nephritis).
Beta-lactam antibiotics are a classic trigger for AIN, characterized by interstitial inflammation often with eosinophiluria.
4
Identify the mechanism of acyclovir-induced nephrotoxicity.
Intravenous acyclovir causes precipitation of insoluble metabolites causing intratubular obstruction.
Acyclovir is poorly soluble in urine and can rapidly form crystals in the tubules, especially in volume-depleted patients, causing intrarenal obstruction.

Key Concept

Mechanisms of drug-induced acute kidney injury (AKI)
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Topics

Nephrology

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