Match each patient's clinical presentation of medication-associated acute kidney injury to the precise pathophysiological mechanism of their renal impairment.
- A 65-year-old man with heart failure with reduced ejection fraction is prescribed indomethacin for an acute gout flare. His serum creatinine rapidly increases. Urinalysis is bland, and the fractional excretion of sodium is 0.4%.Afferent arteriolar vasoconstriction due to inhibition of vasodilatory prostaglandins
- A 72-year-old man with diffuse atherosclerosis and bilateral abdominal bruits is started on lisinopril for hypertension. His serum creatinine rises by 45% over the next week. Urinalysis is unremarkable.Efferent arteriolar vasodilation leading to decreased glomerular hydrostatic pressure
- A 60-year-old woman treated with high-dose intravenous gentamicin for Gram-negative bacteremia develops progressive, non-oliguric acute kidney injury on day 7 of therapy. Urinalysis reveals coarse, muddy brown granular casts.Direct proximal tubular epithelial toxicity causing cellular necrosis and sloughing
- A 48-year-old man receiving intravenous acyclovir for herpes simplex encephalitis develops acute oliguria within 48 hours. Urinalysis reveals red blood cells and birefringent needle-shaped crystals.Intratubular precipitation of poorly soluble drug causing mechanical obstruction
- A 58-year-old man treated with intravenous nafcillin for methicillin-susceptible Staphylococcus aureus bacteremia develops a maculopapular rash and rising creatinine. Urinalysis shows white blood cell casts.Idiosyncratic delayed hypersensitivity reaction causing tubulointerstitial inflammation
Cevap
The correct pairings link NSAIDs to afferent vasoconstriction, ACE inhibitors to efferent vasodilation, aminoglycosides to direct proximal tubular toxicity, acyclovir to intratubular crystal precipitation, and nafcillin to delayed hypersensitivity tubulointerstitial inflammation.
Each presentation maps to a distinct mechanism of medication-induced acute kidney injury. NSAIDs (indomethacin) cause afferent arteriolar vasoconstriction. ACE inhibitors (lisinopril) cause efferent arteriolar vasodilation. Aminoglycosides (gentamicin) cause direct acute tubular necrosis. Intravenous acyclovir causes mechanical obstruction via crystal precipitation. Beta-lactams (nafcillin) trigger immune-mediated acute interstitial nephritis.
Adım Adım Çözüm
Anahtar Kavram
Medication-induced acute kidney injury occurs via distinct pathophysiological mechanisms, including altered glomerular hemodynamics (NSAIDs, ACE inhibitors), direct tubular toxicity (aminoglycosides), tubulointerstitial inflammation (beta-lactams), and intratubular obstruction (acyclovir).
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