A 55-year-old man with a 10-year history of hypertension presents to clinic for follow-up. His blood pressure has been well controlled on lisinopril 10 mg daily (current BP 128/82 mmHg). His primary care physician adds clonidine 0.1 mg twice daily for additional blood pressure control. Two weeks later, the patient reports fatigue, generalized weakness, and mild dyspnea on exertion. Vital signs: BP 124/78 mmHg, HR 54/min, RR 16/min, temperature 37.2°C. Laboratory studies show: serum creatinine 2.3 mg/dL (baseline 0.9 mg/dL), potassium 6.9 mEq/L, BUN 48 mg/dL, urinalysis with no proteinuria or hematuria, and urine output 1.2 L/24 hours. Renal ultrasound shows no obstruction. Which of the following best explains the pathophysiologic mechanism of acute kidney injury in this patient?

1. A)Afferent arteriolar vasoconstriction reducing intraglomerular hydrostatic pressureGABARITO
2. B)Efferent arteriolar vasodilation decreasing glomerular filtration pressure
3. C)Immune-mediated acute interstitial nephritis triggered by clonidine hypersensitivity
4. D)Direct proximal tubule cytotoxicity from clonidine metabolites
5. E)Acute volume depletion and prerenal azotemia from excessive sodium and water loss