Hypertensive Nephrosclerosis and Renovascular Disease

The answer first

Renovascular disease is the great over-imaged and over-stented corner of hypertension. Four rules carry you through the DWE and the long-case defence ^[1]:

1. Look for secondary hypertension with triggers, not by reflex. Young or abrupt onset, truly resistant pressure on three agents including a diuretic, severe hypertension with target-organ damage, or specific clues — a bruit, asymmetric kidneys, recurrent flash pulmonary oedema, a creatinine surge on ACEi/ARB ^{[8] [15]}.
2. The physiology predicts the behaviour. A unilateral stenosis is renin-driven (one-clip physiology); bilateral disease or a stenosed single kidney is volume-driven (two-clip physiology) — and that is why bilateral disease gives you flash pulmonary oedema and sodium retention while unilateral disease gives you high renin and a pressor response to blockade ^[16].
3. For atherosclerotic disease, pills beat stents. CORAL, ASTRAL and STAR all failed to show that adding stenting to optimal medical therapy improves renal function, blood pressure or outcomes — so optimal medical therapy is the default, and revascularisation is reserved for defined subsets ^{[1] [2] [3]}.
4. The exceptions are the exam. Fibromuscular dysplasia in the young woman (angioplasty can cure), bilateral tight stenosis or a single functioning kidney with declining GFR, and recurrent flash pulmonary oedema — these are the patients you revascularise ^{[6] [18]}.

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References24ShowHide

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