A 58-year-old man with a 10-year history of hypertension presents to the emergency department with acute onset severe headache, chest pain, and dyspnea. His blood pressure is 210/140 mmHg. Laboratory investigations reveal: serum creatinine 2.8 mg/dL (baseline 1.0), potassium 5.8 mEq/L, and urinalysis shows 3+ proteinuria with RBC casts. A diagnosis of hypertensive emergency with acute kidney injury is made. An ACE inhibitor is initiated. Which of the following best explains the acute rise in serum creatinine and hyperkalemia immediately after ACE inhibitor administration in this patient?

Explanation

## Mechanism of ACE Inhibitor Effect on GFR and Potassium ### Normal RAAS Function in Hypertensive Crisis In severe hypertension with renal hypoperfusion, the kidneys activate the renin-angiotensin-aldosterone system to maintain glomerular filtration pressure. Angiotensin II preferentially constricts the efferent arteriole, maintaining intraglomerular pressure and GFR despite systemic hypotension or renal hypoperfusion. ### Effect of ACE Inhibitor **Key Point:** ACE inhibitors block the conversion of angiotensin I to angiotensin II, causing selective vasodilation of the efferent arteriole. 1. **Efferent arteriole vasodilation** → decreased intraglomerular hydrostatic pressure 2. **Reduced GFR** → acute rise in serum creatinine (functional/prerenal pattern) 3. **Decreased aldosterone secretion** → reduced potassium excretion in collecting duct → hyperkalemia ### Clinical Context **High-Yield:** This acute rise in creatinine and potassium is **expected and reversible** in the first 1–2 weeks after ACE inhibitor initiation, especially in: - Severe renal hypoperfusion states - Bilateral renal artery stenosis (contraindication) - Advanced CKD with baseline creatinine >2.5 mg/dL **Clinical Pearl:** A rise in creatinine of <30% is generally tolerated and does not mandate discontinuation. However, if creatinine rises >30% or potassium exceeds 6.0 mEq/L, the drug should be held and renal function reassessed. ### Why This Is NOT Increased GFR Afferent arteriole vasodilation (option 0) would increase GFR and is NOT the mechanism of ACE inhibitors — that is the mechanism of vasodilators like hydralazine or nitroprusside. [cite:Harrison 21e Ch 297]