A 62-year-old man with a 10-year history of hypertension and type 2 diabetes mellitus presents to clinic for routine follow-up. He reports dyspnea on exertion over the past 2 weeks and notices bilateral ankle edema. Current medications include lisinopril 10 mg daily for 3 years with well-controlled blood pressure (138/82 mmHg), metformin, and atorvastatin. Vital signs: HR 88/min, RR 18/min, BP 138/82 mmHg, SpO2 98% on room air. Physical examination reveals 2+ bilateral ankle edema and bibasilar crackles. Laboratory studies show: Serum creatinine: 1.8 mg/dL (baseline 1.0 mg/dL 6 months ago) Blood urea nitrogen: 32 mg/dL Serum potassium: 5.8 mEq/L (normal 3.5-5.0) Serum sodium: 138 mEq/L Urine sodium: 45 mEq/day (normal 50-200) Which of the following best explains the development of hyperkalemia and acute kidney injury in this patient?

1. A)Lisinopril blocks angiotensin II formation, leading to decreased glomerular filtration pressure and reduced creatinine clearance, while simultaneously inhibiting aldosterone secretion and impairing renal potassium excretionGABARITO
2. B)Lisinopril competitively inhibits potassium secretion in the proximal tubule while causing direct tubular damage that reduces overall nephron function
3. C)Lisinopril increases angiotensin II levels through negative feedback, which paradoxically promotes glomerular hyperfiltration and hyperkalemia through increased renin release
4. D)Lisinopril activates the sympathetic nervous system, causing intense vasoconstriction of the afferent arteriole and simultaneous stimulation of the collecting duct to reabsorb potassium
5. E)Lisinopril blocks bradykinin degradation, causing vasodilation of the efferent arteriole and hyperkalemia through direct inhibition of Na-K-ATPase