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Estimated Time for Completion: approximately 1 hour
Date of Release and Review: June 1, 2012 and April 2015
Expiration Date: June 1, 2018
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The prevalence of renovascular hypertension depends on one's patient population. It is increased in diabetics, patients with atherosclerotic vascular disease, and the elderly. The natural history of untreated renovascular disease is one of variable progression. One longitudinal retrospective study of hypertensive patients showed that anatomic progression of renovascular disease occurred in only 9.1% of kidneys 1. The pathophysiology of renovascular hypertension revolves around the concept of a critical stenosis. A stenosis of >70%-80% of a vessel lumen is required to produce a "critical" stenosis. When this happens, the renin-angiotensin system and intra-renal pathways are activated and cause arteriolar nephrosclerosis, interstitial fibrosis, and glomerular damage 2. It is important to intervene before irreversible renal damage occurs.
There are two predictors of poor renal outcome and decreased survival after revascularization including an elevated creatinine of >3mg/dL 2. However, dialysis patients have been reported to recover renal function after revascularization. A resistive index of ?0.80 has also been reported to suggest that revascularization would not improve renal function or blood pressure. This is because an elevated RI of ?0.80 reflects irreversible small vessel and parenchymal damage 3. This is controversial because two studies have reported improvement in blood pressure and renal function after revascularization 4,5. So, when is it important to revascularize a patient with renal artery stenosis? As previously mentioned, it is important to understand the likelihood of disease progression. In another prospective study of patients ?65 years of age, progression to a hemodynamically significant stenosis occurred in only 4% of patients at a mean follow up of 8 years 6. It is also important to take into account preexisting co-morbidities including increased age, history of a myocardial infarction, congestive heart failure, and elevated creatinine 7. There are also major procedural complications that can happen after revasculariazation including atheroemboli, artery dissection, hemorrhage, renal perforation, contrast nephrotoxicity, and stent migration or thrombosis 8. Stent restenosis usually occurs within the first year with an incidence of 10%–15%.
Factors that favor medical therapy include well controlled blood pressure with stable renal function, stable renal arterial disease without evidence of progression, advanced age, high risk, limited life expectancy, and significant co-morbidities 9. Factors favoring medical therapy with revascularization include progressive decline in glomerular filtration rate, uncontrolled hypertension despite optimal medical therapy, decline in glomerular filtration rate associated with ACE (angiotensin converting enzyme) inhibition therapy, and recurrent congestive heart failure out of proportion to left ventricular dysfunction 9. However, a few recent studies have raised questions as to the benefits of revascularization. In one study (ASTRAL trial) 806 patients with atherosclerotic renovascular disease were randomized to revascularization (angioplasty ± stent) and medical therapy vs. medical therapy alone. The results of that study suggest there is no clinical benefit from revascularization although there were several study limitations 10. Another trial called the CORAL Trial was recently completed and the data is currently being evaluated. These studies raise questions as to whether the indications for revascularization need further refinement.
Renovascular hypertension can be diagnosed with direct analysis of the main renal arteries evaluating peak systolic velocity and the renal artery to aortic ratio and with indirect analysis in which the segmental renal arteries are evaluated. The latter will be discussed later. When evaluating the main renal arteries, it is important to use color Doppler and obtain angle corrected peak systolic velocities at the origin, mid aspect and distal aspect of the renal artery. Peak systolic velocity should also be recorded at any site of focal color aliasing. Typically the supine or right lateral decubitus positions are used and the vessels may be scanned from an anterior, anterolateral, posterolateral, or coronal approach. The transducer selected for scanning should be based on body habitus. Several articles within the literature suggest that if the peak systolic velocity is between 180 – 200 cm/sec, this is indicative of a stenosis of at least 60% 11-13, (figures 1-4). The renal artery to aortic ratio value has varied in several different articles and is likely 3.0 or less to diagnose a 60% or greater stenosis 12,13,14. There are limitations of direct analysis including multiple renal arteries which may occur in 15%-20% of patients. Scans are also difficult in obese patients due to overlying bowel gas and in the uncooperative patient. Operator experience is invaluable.
Indirect analysis includes evaluating the segmental renal arteries for an early systolic peak, acceleration index and acceleration time 15. It is important to use a posterolateral flank approach and a Doppler angle as close to zero as possible. Evaluation includes obtaining waveforms in the upper, mid aspect, and lower pole of the kidneys with as high a frequency transducer as possible. It is also important to use a fast sweep speed, and appropriate velocity scale and sample volume. An absent early systolic peak has been reported to be very sensitive and specific for diagnosing a renal artery stenosis of ?60% although other authors have not found the early systolic peak to be as sensitive 15-17 (figure 5).
One author reported that the early systolic peak is absent in approximately 50% of normal segmental vessels 18. The acceleration time is the start of systole to the early systolic peak and the acceleration index is the slope from the start of systole to the early systolic peak. When the acceleration time is ?70ms and the acceleration index < 300 cm/sec2, a 60% or greater stenosis can be diagnosed (figure 6).
However, other authors have not found these values to be as sensitive or specific 19,20. One limitation of indirect analysis is that it is not possible to differentiate severe renal artery stenosis from occlusion with collaterals. One endovascular flow wire study that evaluated the early systolic peak, acceleration index and acceleration time found a poor correlation with renal artery stenosis whereas evaluation of the peak systolic velocity and renal artery to aortic ratio using a value of <2 showed excellent correlation with renal artery stenosis 21. A meta-analysis that was recently published involving 88 studies and 8,147 patients found that the peak systolic velocity had the highest performance with a sensitivity of 85% and a specificity of 92% 22. When peak systolic velocity was combined with other parameters, there was little change in accuracy.
Renal vein thrombosis can be due to many causes including nephrotic syndrome, membranous glomerulonephritis, systemic lupus erythematosus, neoplasm, a hypercoagulable state and trauma. It may also be caused by extrinsic compression from inflammatory fluid collections from acute pancreatitis, retroperitoneal fibrosis, hemorrhage, and neoplasm. Acutely patients may present with flank pain and hematuria but if the thrombosis is chronic patients are often asymptomatic. The thrombus may be echogenic, isoechoic, or anechoic and obstructive or non-obstructive (figure 7).
The renal vein may also be enlarged. Acutely, no flow can be detected in the renal vein. However, in patients with chronic renal vein thrombosis, multiple venous collaterals are often visualized as the native kidney can recollateralize within 24 hours (figures 8, 9).
If there is tumor thrombus in the renal vein from renal cell carcinoma, it is important to determine the extent of the thrombus. If it extends into the inferior vena cava or right atrium, or is above or below the hepatic veins, the surgical approach will change (figures 10, 11).
Ultrasound has been reported to be very sensitive and specific for diagnosing renal vein thrombosis.
Arteriovenous fistulas may be caused by penetrating trauma from a stab wound, percutaneous biopsy, or nephrostomy tube placement. Arteriovenous fistulas may also develop secondary to surgery, an inflammatory process, or erosion of an aneurysm into a vein. Some patients may be asymptomatic but can develop hypertension, gross hematuria, urinary tract obstruction from blood clots 23, an elevated creatinine, or high output failure (which is rare). If the arteriovenous fistula is small, it may be observed as it will often spontaneously occlude. If it is increasing in size, coil embolization may be necessary. On ultrasound, increased peak systolic and end-diastolic velocities are noted within the artery and the venous waveform is arterialized 24, (figures 12-14).
There is also surrounding perivascular tissue vibration when the scale is set for low velocity flow.
A pseudoaneurysm may occur due to penetrating trauma from a stab wound, percutaneous biopsy, after a renal transplant, and after nephrostomy tube placement. It may also develop in patients who have undergone a partial nephrectomy or who have a vasculitis or an infection. Certain tumors such as angiomyolipomas also contain pseudoaneurysms. Patients may present with gross hematuria, flank pain, or hypertension 23. If the pseudoaneurysm is small, it may spontaneously thrombose. Coil embolization may necessary if the pseudoaneurysm grows. On duplex and color Doppler, a pseudoaneurysm will have a characteristic to-and-fro arterial waveform within the neck with pandiastolic flow reversal (Figures 15, 16). A yin yang or swirling appearance is noted within the flow lumen of the pseudoaneurysm itself.
In summary, ultrasound is very accurate for diagnosing renovascular hypertension in experienced hands. It is also very accurate for diagnosing renal vein thrombosis, arteriovenous fistula, and pseudoaneurysms.