What are the stages in the pathogenesis of renovascular hypertension (RVHT)?

Updated: Dec 01, 2020
  • Author: Rebecca J Schmidt, DO, FACP, FASN; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Answer

The evolution of RVHT [ref61], [ref62] has been described as having the following three stages or phases:

  1. Renin-angiotensin–dependent phase
  2. Salt-retention phase
  3. Systemic renin-angiotensin–independent phase

In the first phase, the immediate rise in blood pressure is a direct consequence of hyperreninemia. Over days to weeks, blood pressure remains elevated, but the course and presence of hyperreninemia vary with the presence and function of the contralateral kidney. The mechanism by which hypertension is produced in patients with renovascular disease thus changes over time and varies with the state of sodium balance.

When the contralateral kidney is functional, volume expansion is avoided and renin levels remain high. The two kidneys are in opposition; the stenotic kidney avidly retains sodium and produces excess renin in response to renal ischemia, while the nonstenotic kidney excretes sodium and water to maintain euvolemia and renin production decreases. The end result is systemic hypertension that is mediated by both renin and angiotensin.

In the second phase, in the setting of an ischemic solitary kidney, sodium and water retention, together with the vasopressor effects of angiotensin II, act to maintain renal perfusion pressure. The stimulus to produce renin is stifled, and renin levels fall. Hypertension becomes less dependent on angiotensin II and predominantly results from volume expansion. Thus, perfusion pressure is restored at the expense of systemic hypertension and volume overload.

If blood flow is restored during these first two phases and renal perfusion is reinstated, blood pressure soon returns to a normal level. If renal hypoperfusion persists and the third phase is reached, restoration of renal blood flow may not normalize blood pressure, presumably because of secondary irreversible vascular or renal parenchymal disease.

In the third phase, hypertension often is unremitting, persisting well after the removal of the stenosis. Recalcitrant hypertension in this setting likely represents the presence of ischemic nephropathy in either or both kidneys; patients in whom stenoses were not hemodynamically significant initially also may have persistent hypertension.


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