|
|
![]() |
 |
| The Evaluation of the Renal Arteries and Kidneys By: Casey Buckley |
|
Abstract
The renal arteries can be difficult to image due to a number of complications, which include patient body habitus, vessel depth, excessive bowel gas, etc. To familiarize one’s self with the anatomy and ultrasound appearances of the renal arteries can be very helpful. Also being aware of the diseases and abnormalities of these vessels can be very beneficial when evaluating these vessels. Evaluating the renal arteries is very important when determining whether the vessel has a high grade stenosis or if it is completely occluded. Differentiating between the two can help with treatment. |
|
|
Keywords
Renal arteries, Abdominal Aorta branches, kidney |
|
|
Introduction
The renal arteries can sometimes be difficult to image due to patient body habitus, vessel depth, excessive bowel gas, etc. Although protocols may vary from lab to lab, the entire renal artery must be evaluated from the origin off the abdominal aorta to the most distal portion as it enters the hilum of the kidney. A strong good knowledge of the anatomy and physiology, abnormalities, and different diseases of the renal arteries can help the technologist when evaluating these vessels. It has been reported that at least five percent of the population or two to four million people with hypertension has renovascular disease1. |
|
|
 |
| Figure 1: This picture shows the right and left renal arteries branching from the abdominal aorta. |
|
Anatomy and Physiology
The renal arteries branch from the lateral aspect of the abdominal aorta about 1-2 cm distal to the superior mesenteric artery (SMA). The right renal artery courses posterior to the inferior vena cava and is longer than the left renal artery. The left renal artery can be identified by finding the left renal vein, which courses superior to the abdominal aorta and inferior to the superior mesenteric artery, and examining just distal2. The renal arteries enter the kidneys through the hilum and branch into the interlobar arteries, which branch into the arcuate arteries and then finally branch into the afferent glomerular arterioles. Under normal resting conditions, the renal arteries deliver one fourth of the total cardiac output (1200 mL per minute) to the kidneys every minute. Almost 20% of patients will have multiple renal arteries, so the examiner should identify and evaluate each and every one3. There may also be variations with the actual kidney. A normal adult kidney is approximately nine to twelve centimeters (cm) in length, two point five to four cm in depth and four to six cm in diameter. The kidney may reduce in size due to atrophic changes associated with age, circulatory insufficiency, or renal disease. The kidney is composed of two areas, the renal parenchyma and the renal sinus. The renal parenchyma consists of two areas, the cortex which is the outer most section and the medulla which is the inner most portion. The renal sinus is the central most segment of the kidney. The renal sinus contains the hilum, where the renal artery enters and the renal vein exits2. |
|
|
 |
| Figure 2: This image shows the “banana peel” view described in the paragraph. The right renal artery is on top and the left renal artery is on the bottom. |
|
Ultrasound Appearance
To evaluate the renal arteries, place the transducer in a transverse plane, midline of the body. Identify the abdominal aorta and locate the superior mesenteric artery. As stated above, the renal arteries branch just 1-2 cm distal to this artery. In a transverse plane, the abdominal aorta is a circular structure, with the renal arteries demonstrating long tubular structures flowing away from the abdominal aorta4. From a lateral approach and in a longitudinal plane, the “banana peel” image can be seen. On the right side of the patient, just below the rib cage, the abdominal aorta will be rising from the left hand side of the screen to the right. The inferior vena cava can be seen just anterior to the abdominal aorta. The right renal artery will move toward the transducer as a tubular structure and the left renal artery will be coursing away from the abdominal aorta as a tubular structure5. |
|
|
Evaluations
To identify regions of stenosis, look for increases of velocities with post-stenotic turbulence. Normal characteristics of renal arteries have a peak systolic velocity (PSV) of about 100 cm/sec with forward diastolic flow of about 30 cm/sec4. There is continuous diastolic flow which provides the kidney with continuous perfusion. There is also spectral broadening during systole and diastole6. The renal arteries should also have a low resistive index of less than 0.75. Criteria for a greater than 60% stenosis is a PSV greater than 180 cm/sec, with post-stenotic turbulence, dampened waveform in the distal portion of the renal artery and a renal-aortic ratio of greater than 3.5. Renal artery occlusion will have no flow detected and absence of a well visualized renal artery. Also, reduced amplitude color and spectral Doppler signals from the parenchyma will be present. A small kidney size of less than 9 cm may also indicate a renal artery occlusion. |
|
|
Renal Parenchymal Disease
The renal parenchyma is the area from the renal sinus to the outer renal surface. The arcuate and interlobar arteries occupy this space6. In normal kidneys, blood flow in the renal artery is of low resistance. If renal parenchymal disease is present, velocities will be reduced and resistance will be high in the main renal artery and in its branches5. |
|
|
Renal Artery Stenosis
A hemodynamically significant stenosis is considered to be greater than 60%. When a stenosis is present, renal ischemia can occur, which results in a reninangiotensin mechanism and will cause renohypertension. It can also contribute to renal insufficiency by inducing renal parenchymal damage3. As stated above, two to four million people have renovascular disease. The entity is common, patients are typically fifty years of age or older and usually have other atherosclerotic vascular disease. This disease can ultimately produce occlusion in both renal arteries, which eventually causes end stage renal disease (ESRD) 6. |
|
|
 |
| Figure 3: The image below demonstrates the left renal artery completely occluded while the right renal artery is widely patent providing good perfusion to the right kidney. |
|
Renal Artery Occlusion
As stated above, a renal artery occlusion is diagnosed by an absence of a visible renal artery, reduced kidney size, and absence of Doppler signals (both color and spectral) 3. The end result, without some type of medical treatment is ESRD1 |
|
|
 |
| Figure 4: This image shows FMD in the distal portion of the renal artery. |
|
Fibromuscular Dysplasia
This is a disorder of unknown etiology that affects the renal and the internal carotid arteries. Fibromuscular Dysplasia (FMD) affects women (25-50 years old) three times more than men. The renal arteries are the most common site for FMD. The most common clinical symptom is hypertension caused by renal artery stenosis. In the most common form, about 85% of all cases, the media is primarily involved. This particular form of FMD has a characteristic “string of beads” appearance on angiography caused by alternating areas of media fibroplasias and focal aneurysmal dilation5. |
|
|
 |
| Figure 5: This is a picture of acute tubular necrosis. Notice the pale swollen cortex and congested medulla. |
|
Nonvascular Renal Disease
Flow resistance within the renal parenchyma may increase due to much different pathology. These nonvascular renal diseases include urinary tract obstruction, and a host of acute and chronic parenchymal disorders (renal vein obstruction, glomerulosclerosis, acute tubular necrosis, etc). These conditions are all associated with increased flow resistance in the microvasculature of the kidney, which causes the Doppler waveforms to exhibit increased pulsatility5. |
|
|
 |
| Figure 6: The image is of a renal AVF. The feeding artery (A) and vein (V) are seen entering and leaving the origination of the AVF. |
|
Renal ArterioVenous Fistulas
Renal Arteriovenous fistulas (AVF) can be congenital or acquired. Congenital AVFs may be of the aneurysmal or crisoid type. Acquired AVFs are secondary to trauma, surgery, inflammation or can be associated with a neoplasm such as renal cell carcinoma. There can be multiple anechoic tubular structures feeding the malformation with an enlarged renal artery and vein, which increases the blood flow to the kidney. The crisoid type has a characteristic ultrasound appearance of a cluster of tubular anechoic structures within the kidney that are supplied by an enlarged artery and vein. The aneurysmal type is a vascular lesion that should be suspected when the presence of thrombus is noted within a tubular anechoic lumen exhibiting pulsations6. |
|
|
Other Criteria for Diagnosing Renal Artery Stenosis
A renal-aortic ratio (RAR) is a mathematic equation obtained by dividing the highest PSV in the stenotic region (or just the highest PSV if a stenosis is not present) by the PSV of the abdominal aorta at the renal level. A RAR of less than 3.5 is considered normal. This ratio has become a primary criterion for the identification of a significant stenosis. Currently, the theory of this ratio is that it compensates for any hemodynamic variation between patients. Another criterion used is the resistive index (RI). This parameter is not used by itself as a diagnostic tool to rule out renal artery stenosis. However, pulsatility may be evaluated in parenchymal renal disease and urinary tract obstruction. This index may also play a role in predicting responses to revascularization. To mathematically obtain the RI, take the highest PSV of the interlobar and/or arcuate arteries and subtract the end diastolic velocity of the interlobar and/or arcuate arteries and then divide by the same PSV5. There has been research on the resistive index. Mostbeck discovered that heart rate has a statistically significant effect on the RI of renal arteries. Increasing the heart rate of patients and taking measurements at paced race intervals (70, 80, 90, etc) researchers found that the RI decreases with increased heart rate in six of eight patients. They suggested that during the interpretation of the RI in renal arteries, the actual heart rate should always be considered6. |
|
|
Treatment
There are four general therapeutic treatments for patients with renovascular disease. The first is medical therapy to control hypertension, but it does not work if ESRD develops and dialysis is needed. The second type is medical therapy to provide dialysis support if and when the patient develops ESRD. The last two treatments involve the actual attempt to correct the stenosis with percutaneous transluminal angioplasty or surgical revascularization (such as stents). Angiotensin-converting enzyme inhibitors (ACE) may damage already ischemic tissue further, but this risk is counterbalanced by the benefits of this therapy. This ACE inhibitor is not only a potent vasoconstrictor, but also appears to stimulate cell hypertrophy and proliferation. Surgery and angioplasty can preserve or improve renal function and may delay or prevent the need for dialysis. These procedures have lower rates of morbidity and mortality than the ACE inhibitor treatment6. It has been suggested in research that angioplasty of the renal artery can play a greater role in the treatment of patients who have bilateral stenosis rather than unilateral disease 7. However there has also been evidence suggesting that surgical treatments, such as stents, have been more successful than angioplasty. Stent placement has a high success rate and a low rate of re-stenosis. Control of hypertension improves in most patients. Renal function stabilizes or improves in the majority of patients, even those with severe renal failure. These outcomes are maintained over a long period of time 8. |
|
|
Conclusion
Renovascular disease is becoming more common. When evaluating the renal arteries, all aspects of the renal arteries should be observed so diagnosis and treatment can be accommodating to the patient. One should always remember the anatomy and physiology to help visualize the renal arteries. Evaluations of stenosis in renal arteries may vary from lab to lab, however increased velocities with post stenotic turbulence is always an indication of a hemodynamic stenosis. |
|
|
Bibliography
1.) Rimmer, Jeffrey M. and Gennari, F. John. Atherosclerotic Renovascular Disease and Progressive Renal Failure.” Annals of Internal Medicine, 1 May 1993. Vol 118 Issue 9. http://annals.org/cgi/content/full/118/9/712
2.) Curry, Reva Arnez, and Tempkin, Betty Bates. Sonography- Introduction to Normal Structures and Function 2nd Edition. 2004 Saunders, St. Louis, MO.
3.) Fox, Stuart Ira, and Van De Graaff, Kent M. Concepts of Human Anatomy and Physiology 5th Edition. 1999 McGraw-Hill Companies, United States of America.
4.) Daigle, Robert J. Techniques in Noninvasive Vascular Diagnosis- An Encyclopedia of Vascular Testing 2nd Edition. 2002 Summer Publishing, Littleton, CO.
5.) Zwiebel, William J., and Pellerito, John S. Introduction to Vascular Ultrasonography 5th Edition. 2005 Saunders, Philadelphia, PA.
6.) Hagen-Ansert, Sandra L. Textbook of Diagnostic Ultrasonography, 4th Edition, Vol.1. 1995 Mosby, St. Louis, MO.
7.) Casarella, WJ., Martin, LG., and Gaylord, GM. Azotemia Caused by Renal Artery Stenosis: Treatment by Percutaneous Angioplasty.” PubMed 1988 April 15.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=PubMed&list_uids=29...
8.) Tuttle, KR., Chouinard, RF., Webber, JT., Dahlstrom, LR., and Raabe, RD. Treatment of Atherosclerosis Ostial Renal Artery Stenosis with the Intravascular Stent.” PubMed 1998 October.
http://www.ncbi.nlm.gov/enterz/query.fcqi?cmd=retrieve&db=PubMed&list_uids=97...
9.) Marieb, Elaine N. Human Anatomy and Physiology 6th Edition. 2004 Pearson Education INC, San Francisco, CA.
|
|
Copyright CVTC 2003. All Rights Reserved.