ABP Pediatric Nephrology study materials
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Severe Hypertension After Starting an ACE Inhibitor

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Severe Hypertension After Starting an ACE Inhibitor

A 14-year-old girl is referred with recurrent headaches and blood pressure 172/108 mmHg confirmed on three visits. She is not obese, has no family history of hypertension, and has equal arm pressures with normal femoral pulses. Baseline creatinine is 0.9 mg/dL. Because urinalysis shows 1+ protein and she has no edema, she is started on enalapril. Five days later she returns with dizziness and creatinine 2.6 mg/dL, potassium 5.4 mmol/L, and BP 150/96 mmHg. Renal ultrasound reports a right kidney of 8.0 cm and a left kidney of 11.2 cm. She has an abdominal bruit.

1. Explain the physiological reason for her creatinine rise after enalapril and why this points to a specific diagnosis; include what should be done immediately.

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Mechanism. Angiotensin-converting enzyme inhibitors dilate the efferent arteriole and lower intraglomerular pressure. In a kidney with critical renal artery stenosis, perfusion pressure distal to the stenosis is already low; removing angiotensin II–mediated efferent tone causes a sharp fall in GFR. A creatinine rise from 0.9 to 2.6 mg/dL after starting enalapril is therefore a warning sign of renovascular disease.

Why unilateral stenosis can cause this. If the opposite kidney is normal, unilateral stenosis often does not produce global renal failure. This patient's asymmetric kidneys (8.0 vs 11.2 cm) and abdominal bruit suggest right renal artery stenosis, but the acute kidney injury implies bilateral disease or a stenosis in the dominant/left kidney. She needs urgent evaluation.

Immediate actions. Stop enalapril. Assess volume status; avoid NSAIDs and other nephrotoxins. Check electrolytes and creatinine daily. Control blood pressure with a calcium-channel blocker or beta-blocker, not an ACE inhibitor or ARB. Treat hyperkalemia if needed. Do not re-challenge with an ACE inhibitor until renovascular disease is defined.

2. Select antihypertensive therapy while awaiting imaging and explain why ACE inhibitors and ARBs are contraindicated; include a target BP and monitoring plan.

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Drug choice. Use a calcium-channel blocker such as amlodipine as first-line while awaiting imaging because it lowers blood pressure without depending on the renin-angiotensin system. A beta-blocker can also reduce renin release. Thiazides may worsen electrolyte abnormalities and are less ideal in renovascular hypertension. ACE inhibitors and ARBs are contraindicated because they can precipitate acute kidney injury in bilateral renal artery stenosis or stenosis of a solitary/dominant kidney.

Target. Lower blood pressure gradually. For an adolescent with severe symptomatic hypertension, aim for below the 95th percentile (or <130/80 for age 13 or older) over days, not minutes, to avoid cerebral hypoperfusion. Use home BP monitoring and assess for end-organ effects (fundoscopy, echocardiogram, urinalysis).

Monitoring. Check creatinine and potassium 3–5 days after any medication change. Counsel about avoiding dehydration and NSAIDs. If blood pressure remains severe despite two agents, arrange urgent nephrology/hypertension evaluation rather than adding an ACE inhibitor.

3. What imaging strategy would you use and how would you counsel about revascularization versus medical therapy?

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Imaging. Start with renal Doppler ultrasound, recognizing it is operator-dependent and may miss branch disease. Catheter angiography is the gold standard and allows simultaneous intervention; CT or MR angiography can define anatomy but carries contrast or sedation risk. Because she is an adolescent girl, fibromuscular dysplasia is a leading cause.

Revascularization versus medicine. Medical therapy is appropriate for mild stenosis and normal renal function, but severe stenosis, refractory hypertension, flash pulmonary edema, or declining renal function favors revascularization. Percutaneous angioplasty is preferred for fibromuscular dysplasia; surgery is reserved for complex lesions. The small right kidney may already be chronically ischemic.

Counseling. Explain that curing hypertension may not be possible and that long-term surveillance is needed. Discuss risks of angiography, contrast, and angioplasty, and the possibility of restenosis. Avoid ACE inhibitors unless the anatomy is known and a nephrologist is involved.