Renal · Year 2 · from Renal
Case 2: Renal Artery Stenosis
Patient Presentation
A 62-year-old female with a history of smoking presents with difficult-to-control hypertension despite being on three antihypertensive medications including an ACE inhibitor, calcium channel blocker, and thiazide diuretic.
History of Present Illness
- Hypertension diagnosed 3 years ago
- Blood pressure readings consistently >160/95 despite medication adherence
- Recent creatinine increase from 1.0 to 1.6 mg/dL after starting lisinopril
- No symptoms of heart failure
Physical Examination
- Blood pressure: 168/102 mmHg in both arms
- Abdominal bruit heard in the left paraumbilical region
- Peripheral pulses diminished bilaterally
- Evidence of peripheral vascular disease
Workup
Laboratory Studies:
- Serum creatinine: 1.6 mg/dL
- Potassium: 3.2 mEq/L (low)
- Plasma renin activity: Elevated
- Aldosterone: Elevated
Imaging:
- CT angiography: 80% stenosis of the left renal artery at its origin
- Right kidney: 11 cm, normal appearance
- Left kidney: 9 cm (atrophic)
Diagnosis
Atherosclerotic Renal Artery Stenosis
Discussion
This case highlights the unique renal vasculature discussed in the lecture:
- Segmental Arteries: The renal artery divides into five segmental arteries, each supplying a distinct renal segment without collateral circulation - making these end arteries where occlusion leads to infarction
- Two Capillary Beds: The glomerular capillaries (high-pressure filtration) and peritubular capillaries (low-pressure reabsorption) explain why GFR drops when renal perfusion is compromised
- Afferent/Efferent Arterioles: In renal artery stenosis, the kidney depends on angiotensin II-mediated efferent arteriolar constriction to maintain GFR; ACE inhibitors remove this compensation, causing acute creatinine rise
Treatment
- Discontinue ACE inhibitor (creatinine rose >30%)
- Percutaneous angioplasty with stenting considered for refractory hypertension
- Risk factor modification: smoking cessation, statin therapy
- Blood pressure management with calcium channel blockers
Clinical Pearl
The rise in creatinine after ACE inhibitor initiation in this patient is a clue to bilateral renal artery stenosis (or stenosis of a solitary kidney). The normal compensatory response to reduced renal perfusion involves angiotensin II-mediated efferent constriction to maintain glomerular capillary pressure.