|Year : 2004 | Volume
| Issue : 3 | Page : 251-256
|Ultrasound Diagnostic Capabilities in Native Kidney Disease
Molly K House, Robert N Gibson
Royal Melbourne Hospital, Parlville, Victoria, Australia
Click here for correspondence address and email
| Abstract|| |
Renal ultrasound and Doppler studies remain vital diagnostic tools in the evaluation of common renal disorders. It is a non invasive and radiation free tool, which provides anatomical and functional information not provided by other modalities used in isolation. It is a first line tool for many suspected pathologies and is a valuable complementary tool to other modalities.
|How to cite this article:|
House MK, Gibson RN. Ultrasound Diagnostic Capabilities in Native Kidney Disease. Saudi J Kidney Dis Transpl 2004;15:251-6
|How to cite this URL:|
House MK, Gibson RN. Ultrasound Diagnostic Capabilities in Native Kidney Disease. Saudi J Kidney Dis Transpl [serial online] 2004 [cited 2020 Aug 5];15:251-6. Available from: http://www.sjkdt.org/text.asp?2004/15/3/251/32976
| Introduction|| |
Ultrasound evaluation of the kidneys is utilized early in the investigation of acute and chronic renal failure, renal infection and loin pain. B-mode ultrasound provides a useful method for assessing renal size and shape, cortical width and dilatation of the collecting system. Doppler examination of the renal artery and vein, as well as intrarenal vessels is useful for the assessment of stenosis and thrombosis as well as differentiation of acute versus chronic processes. Changes in the intrarenal arterial waveform have been observed in acute obstruction, acute renal vein thrombosis and a number of intrinsic renal disorders.
| Renal Size and Contour|| |
The initial ultrasound assessment of kidneys involves a general overview, including the measurement of bipolar length and the observation of kidney shape. The median bipolar length for a kidney is 11 cm, with a normal range of 9 to 13 cm. Bipolar length correlates most closely with the person's height. 
The kidney size is very useful in determining possible kidney disease. A unilateral small kidney may be caused by post obstructive atrophy, reflux nephropathy, ischemia, renal infarction, radiation nephritis or congenital hypoplasia. Conversely, a unilateral large kidney is seen in compensatory hypertrophy, acutely obstructed kidney, pylonephrosis, duplex kidney and renal tumors. Bilateral small kidneys indicate a chronic process causing renal failure, such as bilateral renal artery stenosis or long standing glomerulonephritis. Bilateral large kidneys are uncommon and are indicative of polycystic kidney disease, proliferative, necrotizing disorders such as Wegener's granulomatosis or polyarteritis nodosa, or infiltration with amyloid or malignant cells in leukemia or lymphoma.
The renal cortex is usually isoechoic, or slightly hypoechoic relative to liver parenchyma. Medullary pyramids are typically hypoechoic to cortex; however, corticomedullary differentiation decreases with increasing age. The central sinus is hyperechoic due to fat, which should be similar in echogenicity to the perirenal fat. The kidney is usually smooth in outline.
The causes of unilateral scarred kidney include reflux nephropathy, tuberculosis, lobar infarction and persistent fetal lobulation. A localized bulge in renal contour may be caused by renal mass or cyst, lobar nephronia, persistent fetal lobulation, or dromedary hump, splenic impression or localized hypertrophy.
| Renal Masses|| |
Ultrasound and computed tomography (CT) are complementary in the assessment of a renal mass.  Ultrasound is less sensitive than CT in the detection of small renal masses, particularly if they are non contour deforming. In masses less than one centimeter, the ultrasound detection rate is approximately 20%; for masses between one and two centimeters, the detection rate is 70%. Ultrasound is very reliable in detecting masses greater than 3 cm. 
Ultrasound is can differentiate cystic from solid masses. A simple renal cyst has strict ultrasound criteria; it should be anechoic, has imperceptibly thin walls, and has posterior wall that is well defined with posterior acoustic enhancement.  A mass with these features can be considered benign and does not require further follow-up.  Any deviation from these strict criteria requires clinical and pathological correlation.
Complex cysts can also be assessed using ultrasound. Suspicious features are similar to the Bosniak criteria used in CT evaluation of complex cysts.  These include multiple septations, particularly if greater than 2 mm thick with internal vascularity. Thickened walls, internal debris, calcification and solid components are also considered suspicious and require CT correlation and assessment.
Up to 10% of renal cell carcinomas have a cystic component. Administration of ultrasound contrast or microbubbles has been shown to improve demonstration of vascularity within cyst septations in a small study of 13 patients. 
Any solid mass must be considered malignant, with the exception of an angiomyolipoma, which has strict ultrasound criteria. Angiomyolipomas are echogenic solid masses. The presence of intratumoral cysts, a hypoechoic rim and/or internal calcification are indicative of a hyperechoic renal cell carcinoma and are rarely demonstrated in angiomyolipomas.  Increased echogenicity has been reported in 61-77% of small renal cell carcinomas, mimicking angiomyolipomas. , CT or MRI correlation is required to demonstrate internal fat.
It is impossible to distinguish between malignant tumors and benign tumors such as adenomas or oncocytomas. Renal cell carcinomas have a variety of sonographic appearances; 50% are hyperechoic, 30% are isoechoic, 10% hypoechoic, and 10% contain cystic components, while 30% have coarse punctate calcification. Doppler can detect internal vascularity and if renal cell carcinoma is suspected the ultrasound evaluation should include the study of the renal vein and inferior vena cava to stage the tumor regarding resectability and vascular invasion.
Ultrasound is notoriously unreliable in the detection of transitional cell carcinomas, particularly in the ureters and lower urinary tract. Occasionally a solid mass arising from the central renal sinus may be demonstrated that may cause focal obstruction.
Non-Hodgkin's lymphoma of the kidney usually manifests as multiple hypoechoic solid masses within the kidney and usually present with metastases in other organs such as the lung, colon and breast; metastases may be solitary and indistinguishable from renal cell carcinoma.
| Renal Infection|| |
In most cases of acute pyelonephritis, the ultrasound examination shows normal kidneys. It is less sensitive than CT or nuclear medicine imaging for the detection of renal cortical inflammatory changes. 
Renal infection may cause an apparent renal mass. These are distinguished from renal cell carcinoma on clinical grounds and require follow-up to exclude malignancy. This so-called lobar nephronia presents as pyelonephritis and is typically a localized area of inflammation.
On ultrasound, a renal abscess may present as poorly defined, complex cystic mass, with internal echogenic fluid. Obstruction of an infected system may lead to pyonephrosis, which appears as a dilated collecting system with internal debris. In more severe emphysematous pyonephrosis, highly echogenic gas may be demonstrated.
Xanthogranulomatous pyelonephritis occurs in renal obstruction secondary to ureteric calculi, and appears as an enlargement and distortion of the renal parenchyma with dilatation of the collecting system and internal debris; extension into the perirenal space may be detected and an echogenic ureteric calculus is usually identified.
Tuberculosis has a number of ultrasound presentations. Hematogenous spread may cause a tuberculoma; it may cavitate into the collecting system causing strictures and calcifications. Furthermore, the direct spread of infection to the ureters and bladder can also result in stricture and calcification.
| Resistive Index|| |
The resistive index is the peak systolic velocity minus the end-diastolic velocity divided by the peak systolic velocity. It is considered a useful parameter for measuring alterations in the renal blood flow that occur with renal disease. 
The resistive index should be measured in the arcuate arteries at the corticomedullary junction or the interlobar arteries at the medullary pyramids. A number of measurements should be obtained and then averaged to obtain a mean resistive index for the imaged kidney.
The mean resistive index in a normal kidney is 0.60, while 0.70 is considered the upper limit of normal. 
The resistive index has been used as an adjunct to B-mode in the work up of renal failure. An initial study demonstrated a normal resistive index in patients with only glomerular dysfunction, compared to patients with interstitial or vascular disease who showed significantly higher resistive index.  Subsequent studies have not supported these findings. 
The resistive index has been shown to be a useful marker for prediction of progression of renal disease , and prediction of recovery of renal function after the treatment of renal artery stenosis. 
| Renal Obstruction|| |
Ultrasound is commonly used to assess for renal obstruction in acute renal failure. Although bilateral renal obstruction causing acute renal failure is uncommon, it is treatable and therefore important to exclude.
Hydronephrosis is described as dilatation of calyces, with demonstration of communication with the renal pelvis and other calyces. Parapelvic cysts and megacalyces are the main differential diagnoses. The causes of hydronephrosis include ureteric obstruction by renal calculi, malignant or infective stricture, retroperitoneal fibrosis, reflux nephropathy or bladder outlet obstruction, most commonly by prostate enlargement.
Traditionally, ultrasound diagnosis of obstruction depends on the demonstration of hydronephrosis. Unfortunately, hydronephrosis is not demonstrated in up to 35% of acute obstruction.  Furthermore, hydronephrosis may be demonstrated in the non obstructed kidney in association with previous obstruction, reflux nephropathy or pyelonephritis. The changes in renal blood flow following acute obstruction have been demonstrated in animal models. ,,, In the initial two hours, vasodilatation is demonstrated due to a prostaglandin release. Vasoconstriction usually follows the vasodilatation with demonstrable decreased renal blood flow and increased vascular resistance, which is due to the mechanical pressure from the obstructed pelvicalyceal system; there is involved interaction between the renin-angiotensin, kallikrein-kinin and prostaglandin-thromboxane systems in this process. ,,,
The initial studies assessing the resistive index as an indicator of acute obstruction showed very promising results with a significantly higher resistive index in the obstructed kidneys; this was corroborated by using CT as the gold standard. , A resistive index greater than 0.7 was reported to be indicative of obstructive disease. The resistive index was demonstrated to return to normal after nephrostomy. Unfortunately, subsequent studies have not demonstrated the same results. In partially obstructed kidneys, the resistive index frequently remains normal. This has been confirmed using animal studies. , In these partially obstructed kidneys, forced diuresis has been used to magnify the change in the resistive index with some success. 
Recent studies have also evaluated the reduction in the venous pulsatility due to loss of compliance of vessels in association with raised interstitial pressure. Whilst an absolute measurement for reduction in venous pulsatility has not been obtained, significant difference between pulsatility in the normal kidney and obstructed kidney has been demonstrated. 
| Renal Artery Stenosis|| |
Doppler ultrasound has been found useful in screening patients with a high pre-test probability of renal artery stenosis. A technically satisfactory study is achieved if the renal artery is successfully interrogated at its origin, mid section and distal portion. Ultrasound contrast agents may help attain a technically satisfactory study and detect accessory renal arteries. ,
Renal artery stenosis has been most successfully diagnosed in the main renal artery. Two parameters are commonly measured; the peak systolic velocity and the renal aortic ratio, which is a measure of the peak systolic velocity in the main renal artery divided by the peak systolic velocity in the aorta at the level of the renal arteries. Using either a peak systolic velocity of greater than 180cm/sec or renal aortic ratio of 3.0 a sensitivity of 85% and specificity of 76% have been achieved to detect significant renal artery stenosis.  This is the authors' preferred approach to ultrasound diagnosis of renal artery stenosis.
Studies have also assessed the intrarenal arteries for significant stenosis as these vessels are easier to image, particularly in the obese patients. By identification of the tardus parvus wave form and associated parameters of acceleration time, acceleration index, acceleration and resistive index and pulsatility index, good detection rates have been achieved.  Unfortunately, these results have not been reproducible.
| Renal Vein Thrombosis|| |
Renal vein thrombosis may be caused by invasion of renal cell carcinoma, compression by tumor or retroperitoneal lymph nodes, extension of inferior vena cava (IVC) thrombus, trauma or renal disease such as amyloid deposition or glomerulonephritis.
Cremin et al  reported a range of ultrasound findings suggestive of renal vein thrombosis. In the early stage, they reported renal enlargement, increased echogenicity, loss of corticomedullary differentiation and hyperechoic streaks in the line of the intralobar vessels. In the second week, the thrombus in the renal vein or IVC was demonstrated with renal enlargement and increased echogenicity in a snowstorm like distribution. Mixed echogenic and hypoechoic areas were demonstrated due to hemorrhage and edema. Late findings included a small kidney with calcification within the kidney or IVC.
As thrombus is not often demonstrated in the early stages, studies have looked at the intrarenal vascular findings to aid early diagnosis. This has proven to be unhelpful in the native kidneys. 
| References|| |
|1.||Emamian SA, Nielsen MB, Pederson JF, Ytte L. Kidney dimensions at sonography: correlation with age, sex, and habitus in 665 adult volunteers. AJR Am J Roentgenol 1993;160:83-6. |
|2.||Kawashima A, Goldman SM, Sandler CM. The indeterminate renal mass. Radiol Clin North Am 1996;34:997-1015 [PUBMED] |
|3.||Besniak MA. The small (less than or equal to 3.0 cm) renal parenchymal tumor: detection, diagnosis, and controversies. Radiology 1991;179:307-17. |
|4.||Goldman SM, Hartman DS. The simple cyst. In: Hartman DS. Renal Cystic Disease. Philadelphia, Pa: Saunders 1989; 6-37. |
|5.||Davidson AJ, Hartman DS, Choyke PL, Wagner BJ. Radiologic Assessment of renal masses: implication for patient care. Radiology 1997;202:297-305. [PUBMED] |
|6.||Bosniak MA. The current radiological approach to renal cysts. Radiology 1986; 158:1-10. [PUBMED] |
|7.||Kim AY, Kim SH, Kim YJ, Lee IH. Contrast-enhanced power Doppler sonography for differentiation of cystic renal lesions: preliminary study. J Ultrasound Med 1999;18:581-8. [PUBMED] [FULLTEXT]|
|8.||Siegel CL, Middleton WD, Teefey SA, McClennan BL. Angiomyolipoma and renal cell carcinoma: US differentiation. Radiology 1996;198:789-93. [PUBMED] |
|9.||Yamashita Y, Takahashi M, Watanabe O. et al. Small renal cell carcinoma: Pathologic and radiologic correlation. Radiology 1992;184: 493-8. |
|10.||Forman HP, Middleton WD, Melson GL, Mcclennan BL. Hyperechoic renal cell carcinomas: increase in detection at US. Radiology 1993;188: 431-4. [PUBMED] |
|11.||Papanicolaou N, Pfister RC. Acute renal infections. Radiol Clin North Am 1996;34: 965-95. [PUBMED] |
|12.||Tublin ME, Bude RO, Platt JF. The resistive index in renal Doppler sonography. Where do we stand? AJR Am J Roentgenol 2003; 180:885 - 92. |
|13.||Keogan MT, Kliewer MA, Hertzberg BS, DeLong DM, Tupler RH, Carroll BA. Renal resistive indexes: variability in Doppler US measurement in a healthy population. Radiology 1996;199:165 -9. [PUBMED] |
|14.||Platt JF, Ellis JH, Rubin JM, DiPietro MA, Sedman AB. Intrarenal arterial Doppler sonography in patients with nonobstructive renal disease: correlation of resistive index with biopsy findings. AJR Am J Roentgenol 1990;154:1223-7. [PUBMED] |
|15.||McDermott R, Teefey S, Middleton W, et al. The resistive index in renal parenchymal disease: no correlation with histopathologic findings. (abstr) Radiology 2000;217(P):560 |
|16.||Platt JF, Rubin JM, Ellis JH. Lupus nephritis: predictive value of conventional and Doppler US and comparison with serologic and biopsy parameters. Radiology 1997;203:82 -6. [PUBMED] |
|17.||Radermacher J, Ellis S, Haller H. Renal resistance index and progression of renal disease. Hypertension 2002;39:699-703. [PUBMED] [FULLTEXT]|
|18.||Radermacher J, Weinkove R, Haller H. Techniques for predicting a favourable response to renal angioplasty in patients with renovascular disease. Curr Opin Nephrol Hypertension 2001;10:799-805. |
|19.||Laing FC, Jeffery RB Jr, Wing VW. Ultrasound versus excretory urography in evaluating acute flank pain. Radiology 1985;154:613-6. |
|20.||Yarger WE, Schocken D, Harris RH. Obstructive nephropathy in the rat: possible role for the rennin-angiotensin system, prostaglandins, and thromboxanes in past obstructive renal function. J Clin Invest 1980;65:400-12. |
|21.||Ichikawa I, Brenner BM. Local intrarenal vasoconstrictor-vasodilator interactions in mild partial ureteral obstruction. Am J Physiol 1979;236:F131-40. [PUBMED] [FULLTEXT]|
|22.||Platt JF, Rubin JM, Ellis JH, DiPietro MA. Duplex Doppler US of the kidney; differentiation of obstructive from nonobstructive dilatation. Radiology 1989;171: 515 -7. [PUBMED] |
|23.||Platt JF, Rubin JM, Ellis JH. Distinction between obstructive and nonobstructive pyelocaliectasis with duplex Doppler sonography. AJR Am J Roentgenol 1989;153:997- 1000. [PUBMED] |
|24.||Cole TC, Brock JW 3rd, Pope JC, et al. Evaluation of renal resistive index, maximum velocity, and mean arterial flow velocity in a hydronephrotic partially obstructed pig model. Invest Radiol 1997;32:154 -60. |
|25.||Coley B, Arellano R, Talner L, Baker KG, Peterson T, Mattrey RF. Renal resistive index in experimental partial and complete ureteral obstruction. Acad Radiol 1995;2:373 -8. |
|26.||Mallek R, Bankier AA, Etele-Hainz A, Kletter K, Mostbeck GH. Distinction between obstructive and nonobstructive hydronephrosis: value of diuresis duplex Doppler sonography. AJR Am J Roentgenol 1996;166:113 -7. [PUBMED] |
|27.||Bateman GA, Cuganesan R. Renal vein Doppler sonography of obstructive uropathy. AJR Am J Roentgenol 2002; 178:921-5 [PUBMED] [FULLTEXT]|
|28.||Melany ML, Grant EG, Duerinckx AJ, Watts TM, Levine BS. Ability of a phase shift US contrast agent to improve imaging of the main renal arteries. Radiology 1997; 205:147-52. [PUBMED] |
|29.||House MK, Dowling RJ, King P. et al. Doppler ultrasound (pre and post-contrast enhancement) for detection of recurrent stenosis in stented renal arteries: preliminary results. Australas Radiol 2000;44:36-40. |
|30.||House MK, Dowling RJ, King P, Gibson RN. Using Doppler Sonography to reveal renal artery stenosis: an evaluation of optimal imaging parameters. AJR Am J Roentgenol 1999;173:761-5. [PUBMED] |
|31.||Stavros AT, Harshfield D. Renal Doppler, renal artery stenosis and renovascular hypertension: Direct and indirect duplex sonographic abnormalities in patients with renal artery stenosis. Ultrasound Q 1994; 89:779-7. |
|32.||Cremin BJ, Davey H, Oleszczuk-Raszke K. Neonatal renal venous thrombosis: sequential ultrasonic appearances. Clin Radiol 1991; 44: 52 - 5. [PUBMED] [FULLTEXT]|
|33.||Platt JF, Ellis JH, Rubin JE. Intrarenal arterial Doppler sonography in the detection of renal vein thrombosis of the native kidney. AJR Am J Roentgenol 1994;162:1367-70. |
Molly K House
Royal Melbourne Hospital, Parkville, Victoria
| Article Access Statistics|
| Viewed||10517 |
| Printed||73 |
| Emailed||0 |
| PDF Downloaded||356 |
| Comments ||[Add] |