From the SIR Residents and Fellows Section (RFS)
Teaching Topic: Treatment of In-Stent Restenosis in Patients with Renal Artery Stenosis
Takahashi E A, McKusick M A, Bjarnason H, Piryani A, Harmsen W S, Misra, S. Treatment of In-Stent Restenosis in Patients with Renal Artery Stenosis. J Vasc Interv Radiol. 2016. 27 (11): 1657 - 1662.
Click here for abstract
In the November 2016 issue of JVIR, a retrospective study examined the clinical outcomes of patients treated for renal artery in-stent restenosis (ISR) with atherosclerotic renal artery stenosis was evaluated. 1,090 renal artery stents were placed in 1,052 patients, with an average patient age of 73.6 years +/- 8.3. in 79 patients, 101 bare metal stents developed ISR, and the patients underwent repeat stent placement vs. angioplasty. Diagnosis of ISR was mainly done via duplex ultrasound. Percutaneous Transluminal Angioplasty and or stent placement was performed. If the patient did not have >30% residual stenosis on follow-angiogram or a mean pressure gradient of < 10 mm Hg, the patient received no further treatment. Otherwise, a bare metal balloon expandable stent was used, with exception of using DES in a small group of patients.
Of the 1,090 renal artery stents, 101 developed ISR. Bilateral ISR was identified and treated in 27.8% of patients. Renal arteries with ISR treated with repeat stent placement were 6.89 times more likely to develop restenosis requiring a repeat procedure compared with arteries treated with PTA (P < 0.01). None of the arteries that received DES during repeat stent placement developed significant restenosis. The study did demonstrate a statistically significant decrease in both SBP and DBP after re-intervention. Of the 101 renal arteries treated for ISR, 13 developed secondary ISR. After ISR treatment, serum creatinine levels improved by a statistically insignificant amount.
In conclusion, treatment of renal artery ISR with PTA among patients with atherosclerotic renal artery stenosis has a lower rate of subsequent ISR compared with repeat stent placement.
1. What is a serious potential setback with renal artery stent placement in patients with atherosclerotic RAS?
When a stent is inserted in an artery, the internal elastic lamina becomes disrupted. This results in smooth muscle cell migration and intimal hyperplasia. These intimal lesions incorporate atherosclerotic elements leading to ISR. In turn, intractable hypertension and renal insufficiency may arise secondary to ISR.
2. Did stent diameter contribute to the rate of restenosis?
The stent or PTA diameter did not have a statistically significant association with renal artery patency. However, there tended to be fewer cases of restenosis with stents or PTA diameters > 5.0 mm. Other studies also found that stent diameter was not a significant predictor of recurrent ISR events, although a similar trend can be seen with increasing vessel diameter related to decreased ISR.
1. What are the two main causes of renal artery stenosis and eventual renovascular hypertension (RVH)?
Atherosclerotic disease and FMD (Fibromuscular Dysplasia).
Other causes include trauma, renal cystic disease, renal cell carcinoma, pheochromocytoma, renal artery aneurysm, reninoma, vasculitis, extrinsic compression and renal infarction.
Source: www.cvphysiology.com
2. What are the imaging modality methods of diagnosing RAS?
Ultrasound with color doppler is the principal tool for detecting RAS / RVH because it is quick, relatively inexpensive and safe. Criteria for significant renal artery stenosis include intrastenotic peak systolic velocity (PSV) of greater than 180 cm/sec and PSV renal/aortic ratio of greater than 3.0 to 3.5.
CT and MRI have been used as a screening exam in some centers, especially if renal function is close to normal. MR Angiography can detect up to 90% to 100% sensitivity and 75-100% specificity. Weaknesses of the method include identification of disease in accessory and segmental renal arteries and artifacts related to metallic clips, intravascular stents or patient motion. Multidetector row CT angiography achieves comparable sensitivity and specificity to MR angiography in depicting renal artery stenosis.
Renal vein sampling measures renin activity in the renal vein vs. the IVC. In a patient with RVH and two functioning kidneys, the affected kidney overproduces renin, and the renin production of the contralateral kidney is reduced. Renal vein renin ratio between the involved and uninvolved kidney of greater than 1.5 and a ratio of (renal renin – IVC renin) / IVC renin of > 0.48 is indicative of RVH.
Lastly, catheter angiography is the gold standard for the diagnosis of RAS. This method allows direct and live visualization of the renal arterial narrowing under fluoroscopic guidance. Hemodynamic significance is proved by the following criteria:
Post author:
Ali Alikhani, MD
Diagnostic Radiology Resident, PGY-4
University of Tennessee Methodist Healthcare
In conclusion, treatment of renal artery ISR with PTA among patients with atherosclerotic renal artery stenosis has a lower rate of subsequent ISR compared with repeat stent placement.
Clinical Pearls
1. What is a serious potential setback with renal artery stent placement in patients with atherosclerotic RAS?
When a stent is inserted in an artery, the internal elastic lamina becomes disrupted. This results in smooth muscle cell migration and intimal hyperplasia. These intimal lesions incorporate atherosclerotic elements leading to ISR. In turn, intractable hypertension and renal insufficiency may arise secondary to ISR.
2. Did stent diameter contribute to the rate of restenosis?
The stent or PTA diameter did not have a statistically significant association with renal artery patency. However, there tended to be fewer cases of restenosis with stents or PTA diameters > 5.0 mm. Other studies also found that stent diameter was not a significant predictor of recurrent ISR events, although a similar trend can be seen with increasing vessel diameter related to decreased ISR.
Questions to Consider
1. What are the two main causes of renal artery stenosis and eventual renovascular hypertension (RVH)?
Atherosclerotic disease and FMD (Fibromuscular Dysplasia).
Other causes include trauma, renal cystic disease, renal cell carcinoma, pheochromocytoma, renal artery aneurysm, reninoma, vasculitis, extrinsic compression and renal infarction.
Source: www.cvphysiology.com
2. What are the imaging modality methods of diagnosing RAS?
Ultrasound with color doppler is the principal tool for detecting RAS / RVH because it is quick, relatively inexpensive and safe. Criteria for significant renal artery stenosis include intrastenotic peak systolic velocity (PSV) of greater than 180 cm/sec and PSV renal/aortic ratio of greater than 3.0 to 3.5.
CT and MRI have been used as a screening exam in some centers, especially if renal function is close to normal. MR Angiography can detect up to 90% to 100% sensitivity and 75-100% specificity. Weaknesses of the method include identification of disease in accessory and segmental renal arteries and artifacts related to metallic clips, intravascular stents or patient motion. Multidetector row CT angiography achieves comparable sensitivity and specificity to MR angiography in depicting renal artery stenosis.
Renal vein sampling measures renin activity in the renal vein vs. the IVC. In a patient with RVH and two functioning kidneys, the affected kidney overproduces renin, and the renin production of the contralateral kidney is reduced. Renal vein renin ratio between the involved and uninvolved kidney of greater than 1.5 and a ratio of (renal renin – IVC renin) / IVC renin of > 0.48 is indicative of RVH.
Lastly, catheter angiography is the gold standard for the diagnosis of RAS. This method allows direct and live visualization of the renal arterial narrowing under fluoroscopic guidance. Hemodynamic significance is proved by the following criteria:
- Reduction in luminal diameter of > 75%.
- Systolic pressure gradient cross stenosis in the main renal artery greater than 10-20mm hg or greater than 20% of aortic systolic pressure.
- A stenosis with a 50-75% reduction in luminal diameter may be hemodynamically significant, but in such cases, pressures should be measured.
Post author:
Ali Alikhani, MD
Diagnostic Radiology Resident, PGY-4
University of Tennessee Methodist Healthcare
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