A 52-year-old woman with a history of recurrent urinary tract infections presents to the emergency department with concern for acute kidney injury. She started trimethoprim-sulfamethoxazole 3 days ago. Vital signs are stable (BP 128/76 mmHg, HR 88 bpm, temperature 37°C). Laboratory studies show serum creatinine increased from baseline 1.0 mg/dL to 1.8 mg/dL; BUN 22 mg/dL; serum potassium 5.8 mEq/L. Urinalysis shows no proteinuria, hematuria, or casts. Renal ultrasound demonstrates normal kidney size, cortical echogenicity, and no hydronephrosis. Urine osmolality is 650 mOsm/kg. The patient reports no fever, flank pain, or dysuria beyond her baseline UTI symptoms. Which of the following best explains the acute rise in serum creatinine with otherwise preserved renal function?
- A)Acute interstitial nephritis from trimethoprim-sulfamethoxazole with immune-mediated tubular injury
- B)Trimethoprim-induced competitive inhibition of creatinine secretion in the proximal tubuleGABARITO
- C)Sulfamethoxazole crystalline nephropathy with intratubular crystal deposition and tubular obstruction
- D)Prerenal azotemia secondary to volume depletion from gastrointestinal losses
- E)Acute tubular necrosis from direct nephrotoxic injury to the thick ascending limb
Explicação
Trimethoprim competitively inhibits organic cation transporters in the proximal tubule that normally secrete creatinine into the urine. This causes an acute rise in serum creatinine without necessarily reflecting a decline in glomerular filtration rate (GFR). ... Ver explicação completa e trilha adaptativa →