A patient with unilateral renal artery stenosis (URAS) has hypertension. Captopril scintigraphy reveals a delayed and diminished tracer uptake in the affected kidney. The mechanism of hypertension in this condition is:
- A Reduced perfusion pressure to the stenosed kidney activates juxtaglomerular cells to increase renin secretion → angiotensin II → systemic hypertension and aldosterone-driven sodium retention ✓
- B Renal ischaemia reduces erythropoietin production, causing anaemia, which reflexively raises cardiac output and blood pressure
- C Reduced GFR in the affected kidney decreases prostaglandin E2 production, removing its vasodilatory effect systemically
- D Activation of renal sympathetic nerves causes afferent arteriolar constriction in the contralateral kidney, reducing its sodium excretion
Explanation
Unilateral renal artery stenosis (Goldblatt 2-kidney 1-clip model) reduces renal perfusion pressure distal to the stenosis. Juxtaglomerular (JG) cells of the affected kidney respond to reduced stretch (baroreceptor mechanism) and reduced sodium delivery (macula densa signal) by markedly increasing renin secretion. Elevated renin cleaves angiotensinogen to angiotensin I → ACE converts it to angiotensin II, which causes: (1) direct vasoconstriction (raised TPR → hypertension), (2) aldosterone release (sodium and water retention), and (3) ADH release. Captopril, by inhibiting ACE and reducing angiotensin II, dramatically reduces GFR in the affected (renin-dependent) kidney, explaining the captopril renography finding. Option D describes a contributing but not primary mechanism; options B and C are incorrect.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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Written and medically reviewed by the StethoPrep medical team.