Editing Renal Hypertension (section)

== Renovascular hypertension ==

=== Background ===

* '''Definition of renovascular hypertension: hypertension due to renal ischemia from partial or complete occlusion of one or both renal arteries'''
* '''Most common form of secondary and potentially curable hypertension'''
** Although renal artery disease affects only a small proportion of hypertensives [majority are primary hypertension], it '''may be the cause of renal failure in as many as 10-20% of patients with ESRD'''

=== Epidemiology ===

* Prevalence similar in Caucasians and African-Americans

=== Etiology of renal artery occlusion ===

* '''Adults (2):'''
*# '''Atherosclerosis'''
*#* '''Most common cause in adults''' (60-80% of all cases)
*#* Accounts for 70% of all renal arterial lesions
*#* '''Usually involves the proximal 1/3 of the renal artery'''
*#** '''In 70-80% of patients, there is an aortic plaque that is impinging on the renal ostium'''
*# '''Fibromuscular dysplasia'''
*#* '''Second most common cause in adults''' (20-40% of all cases)
*#* '''Usually involves the more distal segments of the renal arteries'''
* '''Children (4):'''
*# '''Fibromuscular dysplasia'''
*# '''Vasculitis'''
*# '''Neurofibromatosis'''
*# '''Neuroblastoma'''

=== Pathophysiology of renal hypertension ===

* '''Two-Kidney, One-Clip Model (2K1C) i.e. vasoconstrictor hypertensive model'''
** Because of the ischemia induced by the unilateral stenosis, '''renin secretion is increased from the juxtaglomerular apparatus of the ischemic kidney and suppressed in the normal contralateral kidney.'''
** '''As a consequence of the activation of the renin-angiotensin-aldosterone system (RAAS''') '''and an increased production of angiotensin II, there is peripheral vasoconstriction and hypertension'''
** '''This form of hypertension may be managed with (3):'''
**# '''Reversal of the RAAS (or unclipping of the “clipped kidney”)'''
**# '''ACE inhibitors'''
**# '''Angiotensin receptor blockade'''
* '''One-Kidney, One-Clip (1K1C) Model i.e. volume hypertensive model'''
** There is '''[an initial] activation of the RAAS''' similar to that seen in the 2K1C model. However, in contrast to the 2K1C kidney, '''the absence of a normal contralateral kidney prevents an ensuing natriuresis and diuresis. Thus, there is''' '''volume expansion, and renin secretion is suppressed in the clipped kidney''' because of feedback inhibition. Volume expansion remains, and there is '''sustained hypertension in spite of the decreased vasoconstriction''' associated with the now '''suppressed RAAS.'''
** '''1K1C model is driven by volume expansion and sodium retention with normal circulating levels of angiotensin II.'''

=== Pathophysiology of Ischemic Nephropathy ===

* '''In addition to hypertension, renal artery stenosis (RAS), when hemodynamically significant, affects the entire renal functioning parenchyma and causes ischemic nephropathy'''
** '''It is unlikely that the renal damage observed in RAS is secondary to the decrement in renal blood flow (RBF) alone. The secretion of proinflammatory mediators released as a consequence of the stenosis is likely the more significant causative factor.'''
** The poststenotic renal parenchyma demonstrates a mixture of vascular sclerosis, cholesterol crystals, tubular atrophy, interstitial fibrosis with inflammatory cells, atubular glomeruli, and focal or global glomerulosclerosis
* '''The degree of stenosis necessary to produce a hemodynamically significant effect (reduction in RBF > 40%) has been estimated at 70-80%, and thus this percent of stenosis is referred to as a “critical stenosis”'''
** '''With > 80% stenosis, perfusion pressure will drop to < 70-80 mm Hg, at which point the kidney can no longer autoregulate its GFR and RBF'''
* '''Renovascular hypertension is more likely to be observed when (2):'''
*# '''≥ 70% stenosis in one or both renal arteries'''
*# '''50% stenosis with post-stenotic dilatation'''

=== Diagnosis and Evaluation ===

==== History and Physical Exam ====

* '''Most patients with renovascular hypertension present with moderate to severe hypertension'''
* '''Signs and symptoms of underlying possible renovascular disease and need for further evaluation if warranted (8):'''
*# '''Severe or refractory hypertension with evidence of''' grade III or IV '''hypertensive retinopathy''' (particularly in Caucasians)
*# '''Abrupt onset of moderate to severe hypertension''', particularly in a normotensive or previously well-controlled hypertensive
*# '''Onset of hypertension before age 20''' (early onset) or after age 50 (late onset), particularly in those without a family history of hypertension
*# '''Unexplained worsening of renal function (with or without hypertension) in association with the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs)''' or with a reduction of blood pressure to the current accepted norm with the use of other antihypertensive agents
*# '''Paradoxic worsening of hypertension with the use of diuretics'''
*# Unexplained recurrent episodes of heart failure—“flash” pulmonary edema
*# The presence of a systolic-diastolic abdominal bruit that radiates to both flanks
*# The presence of diffuse vascular disease and/or evidence of cholesterol embolization

==== Imaging ====

* '''Screening Tests'''
** '''The screening tests that provide the highest sensitivity and specificity are (3):'''
**# '''Magnetic resonance angiography (MRA)'''
**# '''Computed tomography angiography (CTA)'''
**# '''Duplex Doppler US'''
*** '''Renal scintigraphy is no longer recommended as a screening test to establish the diagnosis of RAS.'''
*** '''CTA and MRA do not visualize the distal renal arterial tree well'''
*** A transient deterioration of renal function is not infrequently seen following a contrast load in patients with significant RAS and limited renal function
** '''MRA with Gadolinium'''
*** '''May be used as a highly sensitive and specific non-invasive test to assess the functional significance of a renal vascular lesion; both the RBF and the GFR can be determined by the study digital subtraction angiography (DSA)'''
*** '''Concerns regarding the possibility of gadolinium-induced nephrogenic systemic fibrosis have diminished its utility in those with unstable or reduced renal function (GFR <30 mL/min).''' In these patients, a non-contrast MRA study may be performed, but this shows far less sensitivity and positive predictive value than a gadolinium-enhanced study
** '''CTA'''
*** Limited in those with renal insufficiency because both the sensitivity and specificity declines in the presence of renal insufficiency (serum creatinine >1.7 mg/dL), and the risk of dye-induced nephrotoxicity increases
** '''Duplex Doppler US'''
*** '''The most important indicator of renal artery stenosis is increased peak systolic velocity (PSV > 180cm/sec)'''
*** Similar to MRA, duplex Doppler US provides both anatomic and functional information.
*** Disadvantages:
**** Time-consuming
**** Highly operator dependent
**** Technically difficult test to perform
*** The sensitivity of this technique may be further increased when ACE inhibition is used  

* '''Confirmatory test'''
** '''Angiography'''
*** '''Despite a negative screening test, renovascular disease may still be present, particularly if the lesion is in the distal or intrarenal portion of the artery.'''
*** '''Both conventional renal angiography and intra-arterial digital subtraction angiography remain the gold standard for diagnosing renovascular disease and are indicated if the clinical index of suspicion is high and intervention is contemplated, regardless of the outcome of the screening tests'''