When aortic dissections extend to the renal arteries, reductions in renal blood flow can cause marked increases in renin production. The resultant rise in angiotensin II can lead to difficult-to-control blood pressure, despite normal postdissection antihypertensive agents. We highlight a case of a postdissection patient with malignant hypertension refractory to eight different enteral antihypertensives. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers had been held due to postoperative acute kidney injury. A single dose of valsartan, administered on day 12, produced a marked drop in blood pressure, alleviation of encephalopathy, and allowed for cancellation of a planned tracheostomy. A serum renin level was found to be 50 times the normal upper limit. In patients with aortic dissection and renal artery involvement, angiotensin-modifying agents may warrant earlier administration to combat this unique cause of hypertension.
Keywords: aortic dissection; hypertension; pharmacology; renal artery; renin-angiotensin-aldosterone system.
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