A 68-year-old man with stage 4 chronic kidney disease (baseline creatinine clearance 22 mL/min) presents with dysuria, urinary frequency, and suprapubic pain. Urinalysis shows pyuria and bacteriuria; urine culture grows E. coli. He is initiated on gentamicin 5 mg/kg intravenously once daily for presumed urosepsis. After 3 days of treatment, his serum creatinine increases from 2.6 to 4.1 mg/dL, and urine output decreases from 800 mL/day to 350 mL/day. Urinalysis now reveals muddy brown casts and epithelial cell casts. His vital signs remain stable (BP 136/80, HR 88, RR 14, temperature 37.1°C), and he denies fever, rash, or new flank pain. Which of the following best explains the mechanism of renal injury in this patient?
- A)Gentamicin-induced membranoproliferative glomerulonephritis causing immune complex deposition
- B)Acute interstitial nephritis from drug hypersensitivity with eosinophiluria and fever
- C)Aminoglycoside accumulation in proximal tubule cells with inhibition of protein synthesis and cell deathGABARITO
- D)Crystalline nephropathy from precipitation of gentamicin metabolites within the distal convoluted tubule
- E)Direct glomerular capillary injury from high serum gentamicin levels causing proteinuria
Explicação
Aminoglycosides cause dose-dependent, non-oliguric acute kidney injury through proximal tubule toxicity. Gentamicin is filtered at the glomerulus and taken up by proximal tubule cells via endocytosis, accumulating in lysosomes where it inhibits mitochondrial p... Ver explicação completa e trilha adaptativa →