What is the role of renovascular hypertension (RVHT) in chronic kidney disease?

Updated: Dec 01, 2020
  • Author: Rebecca J Schmidt, DO, FACP, FASN; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Since the seminal experimental work by Goldblatt and colleagues in 1934, [4] RVHT has increasingly been recognized as an important cause of clinically atypical hypertension and chronic kidney disease, the latter by virtue of renal ischemia. RVHT is the clinical consequence of activation of the renin-angiotensin-aldosterone system (RAAS).

Renal artery occlusion creates ischemia, which triggers the release of renin and a secondary elevation in blood pressure. Hyperreninemia promotes conversion of angiotensin I to angiotensin II, causing severe vasoconstriction and aldosterone release. The ensuing cascade of events varies, depending on the presence of a functioning contralateral kidney.

When two kidneys are present, aldosterone-mediated sodium and water retention is handled properly by the nonstenotic kidney, precluding volume from contributing to the angiotensin II–mediated hypertension. By contrast, a solitary ischemic kidney has little or no capacity for sodium and water excretion; allowing volume to play an additive role in the hypertension.

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