Reno vascular Hypertension

Reno vascular Hypertension
(Prof. Dr. Sherif Mokhtar, MD Professor of Cardiology & Critical Care Medicine Cairo University )
Renal Artery Stenosis (RAS) may result in hypertension and/or ischemic nephropathy, eventually leading to end-stage renal disease (ESRD). It affects RAS is due to atherosclerosis in about 90% of cases, and usually involves the ostium and proximal third of the main renal artery and the perirenal aorta. Segmental and diffuse intrarenal atherosclerosis occurs less frequently and usually represents advanced disease. Similar to other atherosclerotic disease RA, occurs in middle age and beyond, and is most common in patients with aortoiliac occlusive disease, diabetes, CHD, and/or tobacco use.
The remaining 10% or so of RAS is caused by Fibromuscular Dysplasia, a type of vasculitis that affects one or more layers of the renal artery, usually including the media. It more often affects younger persons, particularly women, and involves the distal 2/3 of the renal artery, and is less likely to progress than atherosclerotic RAS, although the intimal and periarterial forms are associated with dissection and thrombosis.
Angiographic Appearance of the Two Most Common Forms of Renal-Artery Stenosis:
Panel A shows the typical beaded, aneurysmal appearance of the distal right renal artery in a patient with refractory hypertension and fibromuscular dysplasia.
After angioplasty, Panel B shows there was improvement in the angiographic appearance and resolution of hypertension.
Panel C shows the typical appearance of atherosclerotic renal-artery stenosis, involving the ostium and proximal third of the left renal artery (arrows).
Clinical Features Suggestive of Renovascular Hypertension:
1. Severe or Refractory Hypertension, with evidence of Grade III or IV hypertensive retinopathy (particularly in Caucasians).
2. Abrupt Onset of moderate to severe hypertension, particularly in a normotensive or previously well-controlled hypertensive patient.
3. Onset of hypertension before age 20 (“early onset”) or after age 50 (“late onset”), particularly in those without a family history of hypertension.
4. Unexplained worsening of renal function:
a) With or without hypertension, or
b) In association with the use of ACEI or ARBs, or
c) With reduction of BP to the current acceptable norm with the use of other antihypertensive agents.
d) Increase of ● 30% in serum creatinine after starting ACE inhibitor or ARB.
e) Paradoxical worsening of hypertension with diuretics.
f) Unexplained recurrent episodes of heart failure – “flash” pulmonary edema.
5. Systolic-diastolic abdominalbruit, which radiates to one or both flanks.
6. Diffuse vascular disease and/or cholesterol embolization.
7. Unilateral small kidney on imaging.
Work Up for Atherosclerotic RAS:
● Should be done only if there is resistant hypertension or
● If there is worsening renal function, and
● If there is no contraindication to an invasive procedure (percutaneous transluminal renal angioplasty, PTRA, with or without stenting, or revascularization surgery), and
● If the patient is willing to accept revascularization.
● Otherwise, only medical management is advised.
Diagnosis of Reno-vascular HTN:
Measurements of peripheral venous plasma renin activity (PRA) at rest or following stimulation with ACE inhibitors,
● Lack the sensitivity and specificity to be useful in screening for RAS.
● Moreover, in the chronic stages of hypertension, PRA may be suppressed due to volume overload, and the hypertension may not be angiotensin dependent.
Noninvasive tests for RAS:
● Radioisotope scanning with ACE inhibition (captopril scintigraphy),
● Doppler ultrasound,
● MR angiography (MRA), and
● CT angiography.
The sensitivity of these imaging techniques varies from 80-95% under optimal conditions, but each has its advantages and limitations.
Captopril Scintigraphy:
● Noninvasive, relatively inexpensive, and avoids exposure to potentially nephrotoxic contrast agents. But does not delineate the anatomy of the vascular bed.
● Less accurate in bilateral disease or advanced renal failure because it depends on a difference in isotope uptake between the two sides.
Doppler ultrasound is highly operator dependent and technically difficult to perform, especially in the presence of abdominal obesity and bowel gas.
MRA and CTA produce excellent image quality, but are expensive.
MRA produces poor images with stents or distal stenoses (as in fibromuscular dysplasia), and CTA requires contrast medium, often contraindicated in renal insufficiency.
Renal Arteriography
● The definitive diagnostic test for RAS,
● Indicated if the clinical index of suspicion of RAS is high, and intervention is contemplated because of resistant hypertension or deteriorating renal function.
● Revealing in addition the extent of intrarenal and associated aortic vascular disease and the dimensions of the kidneys. Reno-vascular Hypertension Treatment The choice of therapy is dictated by: 1- Whether the lesion is atherosclerotic or fibromuscular, 2- Its proximity to the renal ostium, 3- The extent of renal arterial involvement, 4- The patient’s comorbid medical condition(s), 5- The ease or difficulty in controlling hypertension and preventing progressive renal insufficiency with drugs alone and 6- The inherent risks, as well as the skill of available operators in performing interventional procedures. PTRA If Unsuccessful Proceed with Surgery in those patients with: ● Unilateral RAS and/or without either significant comorbid conditionsor diffuse vascular disease; consider and proceed in those select high-risk patients.
Post PTRA HTN may be explained by:
● Residual Ischemic Nephropathy in the affected kidney, maintaining the renal hypertension,
● Restenosis of the affected kidney, or
● Progression of atherosclerotic disease in the contralateral kidney.
PTRA in Fibromuscular Dysplasia
● PTRA is the treatment of choice for patients with fibromuscular dysplasia,
● Technical success rate of 87-100%,
● A favorable effect on BP of 90%,
● A restenosis rate of only 10%, and a 10-year success rate of 90%.
Medical Therapy
Control of BP may be achieved in ●90% of cases with medical therapy alone, usually with a combination of antihypertensive drugs.
All classes of these drugs may be used, but drugs that inhibit angiotensin II production or block its receptor are particularly effective.
This should be augmented with antiatherosclerotic and antithrombotic measures such as statin therapy, smoking cessation, and aspirin.
Angiotensin II has a greater vasoconstrictor effect on the efferent arteriole than on the afferent arteriole, and
Thus is responsible for the maintenance of glomerular filtration pressure, and therefore of glomerular filtration rate.
ACEIs and ARBs will cause a fall in glomerular filtration pressure and GFR, and consequently, an increase in the serum creatinine.
This is a normal response to these drugs, and is not an indication to discontinue them, unless the fall in GFR or the increase in serum creatinine is > 30% from baseline (if the baseline creatinine is ≤3 mg/dl).
In rare cases, acute (usually reversible) renal failure may occur, suggesting the presence of:
● High-grade lesion,
● RAS accompanied by severe renal parenchymal disease,
● Volume contraction, or
● Occult heart failure.
Renal function should be carefully monitored whenever ACEIs or ARBs are used in patients with RAS, particularly when combined with a diuretic.
Most patients with atheroscleroticRAS require medical antihypertensive therapy as either primary treatment or following PTRA because the Revascularization alone is seldom sufficient to control BP in middle-aged or elderly patients with RAS.
Surgical Revascularization
● Seldom indicated in fibromuscular hyperplasia because PTRA is so successful in this condition,
● Not recommended as initial therapy for control of BP in patients with atherosclerotic RAS because of high rates of morbidity/mortality associated with the procedure in these patients, and
● Because modern medical antihypertensive therapy is so successful.
Surgical revascularization should be reserved for patients with:
● Aortic disease or
● Failed PTRA, with or without stenting,
● For preservation of renal function and
● For BP control.
Determinants of Revascularization Outcome
The success of surgical and catheter-based revascularization in preserving renal function depends on the:
● Adequacy of the vasculature distal to the site of the arterial lesion,
● The level of renal function at the time of intervention, and
● The rate at which renal function has deteriorated prior to intervention.
Best results are achieved with serum creatinine Medical vs Revascularization Therapy
● Medical therapy is the treatment of choice for hypertension in patients with atherosclerotic RAS, particularly if BP and renal function can be controlled.
● The severity of RAS is closely related to total atherosclerotic burden, and advanced atherosclerosis has an overriding mortality risk that may be only minimally affected by renal artery revascularization.
● It is not clear whether renal revascularization, by whatever means, changes the natural history or mortality of patients with atherosclerotic RAS.
● Small prospective, randomized trials comparing medical therapy with either surgical or endovascular treatment have not found differences in renal survival or mortality.