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Invited Commentary |

The Kidney Connection Holy Grail or Wild Goose Chase?

David M. Safley, MD1,2; Adnan K. Chhatriwalla, MD1,2
[+] Author Affiliations
1Saint Luke’s Mid America Heart Institute, Kansas City, Missouri
2University of Missouri–Kansas City, Kansas City
JAMA Intern Med. 2014;174(11):1851-1852. doi:10.1001/jamainternmed.2014.3139.
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The pathophysiologic mechanisms of renovascular hypertension are well described: Hemodynamically significant renal artery stenosis results in reduced renal perfusion pressure, which in turn leads to activation of the renin-angiotensin system and increased levels of angiotensin II, resulting in systemic vasoconstriction, aldosterone release, sodium retention, and expansion of extracellular fluid volume and blood volume. Logically, reversal of the restriction in flow and establishment of normal renal perfusion pressure should reverse the process and decrease blood pressure. Nevertheless, the clinical benefits of renal artery revascularization in the setting of refractory hypertension have been variable, and largely disappointing.

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