## Clinical Context This 52-year-old man with known essential hypertension presents with **inadequately controlled BP** (156/96 mmHg on amlodipine monotherapy), **acute worsening of renal function** (creatinine 1.0 → 1.8 mg/dL over 6 months), **new 2+ proteinuria**, fatigue, and ankle edema. The most appropriate next step is to **add an ACE inhibitor (lisinopril) for renoprotection and arrange a renal ultrasound** to evaluate the structural basis of the acute kidney injury. ## Why Option B Is Correct **Key Point:** In a hypertensive patient with **new proteinuria and rising creatinine**, ACE inhibitors (or ARBs) are the **first-line renoprotective agents** — they reduce intraglomerular pressure, decrease proteinuria, and slow progression of hypertensive nephropathy (Harrison's Principles of Internal Medicine, 21st ed.; JNC 8 guidelines). 1. **Proteinuria + hypertension = ACE inhibitor indication:** Proteinuria signals glomerular injury. ACE inhibitors reduce efferent arteriolar tone, lowering intraglomerular pressure and proteinuria. This is a well-established, guideline-backed intervention. 2. **Renal ultrasound is appropriate:** A renal ultrasound evaluates kidney size, echogenicity, cortical thickness, and hydronephrosis — all relevant to acute-on-chronic kidney disease. It is the standard first-line imaging for new renal dysfunction. 3. **The clinical picture is NOT classic RAS:** The patient has a known diagnosis of essential hypertension and a gradual creatinine rise over 6 months (not an acute post-ACE inhibitor rise). There is no mention of an abdominal bruit, flash pulmonary edema, or resistance to ≥3 antihypertensives — the hallmarks that mandate RAS workup before ACE inhibitor use. ## Why Option C Is Incorrect **High-Yield:** Renal artery Doppler + plasma renin activity (Option C) is indicated when RAS is **strongly suspected** — i.e., resistant hypertension (≥3 drugs), abdominal bruit, flash pulmonary edema, or acute creatinine rise after ACE inhibitor initiation. In this patient, none of these classic RAS triggers are present. Jumping to RAS workup before initiating guideline-directed therapy (ACE inhibitor + structural imaging) is premature and not the "best next step." **Clinical Pearl:** The concern that "ACE inhibitors are contraindicated until RAS is excluded" applies to patients with **bilateral RAS or RAS in a solitary kidney**, or those with strong clinical suspicion of RAS. In a patient with proteinuric hypertensive nephropathy without RAS red flags, withholding ACE inhibitors causes harm by allowing ongoing glomerular injury. (Kaplan's Clinical Hypertension; Harrison's, 21st ed.) ## Why Other Options Are Wrong | Option | Why Incorrect | |--------|---------------| | Increase amlodipine to 10 mg | Calcium channel blockers have no renoprotective effect on proteinuria; does not address the glomerular injury. | | Renal artery Doppler + plasma renin (Option C) | Appropriate only if RAS is strongly suspected; premature here without classic RAS features. | | Start dialysis | Grossly premature; eGFR ~35–40 mL/min (CKD Stage 3b), far from dialysis threshold. | ## Summary **Best next step = Add lisinopril (renoprotection + BP control) + renal ultrasound (structural evaluation of AKI).** This is the guideline-concordant approach for a hypertensive patient with new proteinuria and rising creatinine without classic RAS features. (Harrison's 21st ed.; KDIGO CKD Guidelines 2022)
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